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Lecture 5b 4 Feb 2013
Atherosclerosis-Nutritional intervention-emphasis should be on prevention-
Group activity
A patient presents with severe atherosclerosis
(severe stenosis and accompanying chest pains).
From a clinical perspective is diet modification
alone the best approach to reducing the risk of MI?
Why or why not?
If not then what are the other medical
options available?
Lipids
LCAT preference for GLA > LA > OA > AA>
DHA
LPL-preferences increase activity-no reports
found
CETP-preferences increase activity-no reports
found
Blood Levels of concern- new ATP-NCEP
guidelines issued 2004-diet approaches are
constantly changing
HDL
LDL
Addressed when triglycerides are
addressed
including oxidized LDL
Table 6, Fig 1,2 ATP
main target of diet
Blood Levels of concern
Lp(a)- diet does not alter (very tight genetic
control)
Cholesterol
-addressed when LDL is addressed
TriglyceridesFasting plasma-fish is an option, reduction
in saturated fat-frequently dietary
recommendations for LDL also take
care of triglycerides
Blood Levels of concern
Triglycerides
-post-prandial-fish is an option –what does this
say about LPL?
HDLc: LDLc ratio of < 0.2 – again emphasis is on
LDL first
Blood Levels of concern
Triglycerides and small dense LDL
As plasma triglyceride levels fall there is a
smaller percentage of small dense LDL
-reduce triglycerides as above
Triglycerides and low HDLc
-this is due to low LPL activity
-reduce triglycerides as above
Macrophages
Increase b-carotene, vitamin E and C-jury is still
out on these issues?
Platelets
Platelet membrane fatty acid composition
Phospholipase A2 and Cyclooxygenase
Platelets
Platelet membrane fluidity-reduce saturated fat
and dietary cholesterol since they both decrease
membrane fluidity
Platelets- Interaction with lipoproteins
HDL-lowers aggregation-no observed impact of
nutrition (no studies done) here
LDL-elevates aggregation-no observed impact of
nutrition (no studies done) here
Lp (a)-depresses platelet aggregation though
also thought to inhibit plasminogen
activation no observed impact of
nutrition (no studies done) here
Blood pressure
Reduce saturated fats and dietary
cholesterol and increase pufa to
improve artery patency
-remember that plaque formation’s
sequelae include calcium
deposition that further reduces
artery patency
Obesity
-diets high in oleic acid (18:1 n-9) MAY result in
weight loss
Renal Disease
-see blood pressure
Various Pathogens
Adequate nutrient intake is critical to
maintaining immune response
Nitric oxide
-vasodilation, antiplatelet effects, also
important in immune response
-high salt intake in salt sensitive individuals
reduces NO production and may
explain increased blood pressure due
to NO factor
-may also explain why MUFA lowers blood
pressure
-increased blood pressure can result in
increased platelet reactivity
Nitric oxide
decrease NO production can result in decreased
immune response (pathogen impact)
Diet drug interactions
Cholestyramine-lowers cholesterol by acting as a
bile acid sequestrant -nausea, GI distress and
constipation and can lead to fat soluble vitamin
deficiencies
Colestipol -lowers cholesterol by acting as a bile
acid sequestrant is less likely than
cholestyramine to cause the above problems but
it can give constipation
Diet drug interactions
Gemfibrozil - speeds up LPL action on VLDL
and hence reduces triglycerides-can lead to
nausea and GI distress
Statins (cholesterol lowering HMG-CoA
synthase inhibitors)-lovastatin, pravastatin,
simvastin) should not be given with grapefruit
juice
Limit alcohol content
Diet drug interactions
Anticoagulants (eg aspirin) and hyper doses of
vitamin E (> 2000 IU/day) should be limited
-Coincidental high intakes of fish-to be
avoided
-aspirin inhibits platelet function by inhibiting
cyclooxygenase
Aspirin can lead to folate and vitamin C
deficiencies (potential heart
disease consequences?)