ODS Eicosanoids Home
Events linking diet and
disease
Cardiovascular death occurs with thrombosis and
arrhythmia, often after years of progressive vascular inflammation. Two chronic dietary imbalances lead to these
conditions: excess food energy intake
over expenditure and excess intake of omega-6 (n-6) over omega-3 (n-3)
fats. Each imbalance can be readily
prevented.
Meals
with excess food energy
increase production of plasma triglycerides (fats)
which circulate and form non-esterified fatty acids
(NEFA) that stress vascular walls. In
addition, unburned sugar and fat increase cytosolic
levels of acetyl-CoA, HMG-CoA
and mevalonate and lead to prenylated
proteins that impair beneficial nitric oxide actions
and increase inflammatory/proliferative vascular
events. Nitroglycerin provides nitric oxide to impaired vessels and aspirin
cuts n-6 eicosanoid-driven thrombosis.. Plasma cholesterol is more a marker of excess mevalonate than a mediator of vascular injury,
and statin has anti-inflammatory action by inhibiting
mevalonate formation. The medications treat events
driven by the two readily prevented nutritional imbalances in the upper left of
the figure.
Chronic
dietary shortages of n-3 fats create high proportions of n-6 highly unsaturated
fatty acids (HUFA) in tissue phospholipids that enhance the intensity of n-6 eicosanoid-mediated inflammation, thrombosis and
arrhythmia. Eating less food energy per meal and eating more n-3 and less n-6
fats are useful primary steps for preventing risk. To see slide show of the above image please select the following link:
Chain of Events