1. Lecture 5b 7 Feb 2011
Atherosclerosis-Nutritional intervention-
-emphasis should be on prevention-

2. 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?

3. Lipids
LCAT preference for GLA > LA > OA > AA> DHA
LPL-preferences increase activity-no reports found
CETP-preferences increase activity-no reports found

4. Blood Levels of concern- new ATP-NCEP guidelines issued 2004-diet approaches are constantly changing
HDL
Addressed when triglycerides are addressed
LDL
including oxidized LDL
Table 6, Fig 1,2 ATP
main target of diet

8. Blood Levels of concern
Lp(a)- diet does not alter (very tight genetic control)
Cholesterol
-addressed when LDL is addressed
Triglycerides-
Fasting plasma-fish is an option, reduction in saturated fat-frequently dietary recommendations for LDL also take care of triglycerides

9. 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

10. 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

11. Macrophages
Increase B-carotene, vitamin E and C-jury is still out on these issues?

12. Platelets
Platelet membrane fatty acid composition
Phospholipase A2 and Cyclooxygenase

13. Platelets
Platelet membrane fluidity-reduce saturated fat and dietary cholesterol since they both decrease membrane fluidity  

14. 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

15. 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

16. -diets high in oleic acid (18:1 n-9) MAY result in weight loss
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

17. 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

18. Nitric oxide
decrease NO production can result in decreased immune response (pathogen impact)

19. 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

20. Diet drug interactions
Gemfibrozil - speeds up LPL action of 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

21. 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?)