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Do Polyunsaturated Fatty Acids Protect Against Heart Disease?


There are many known risk factors associated with cardiovascular disease (CVD); such as, diet, high blood pressure, sedentary lifestyle, obesity and heredity.  Two of the main biochemical risks are high plasma low-density lipoprotein cholesterol (LDL) and low plasma high-density lipoprotein cholesterol (HDL).  LDLs are the major transporter for cholesterol to tissues.  Circulating LDLs bind to specific LDL receptors on cell surfaces, and the LDL is internalized and degraded by the cell.  Both the protein and lipid components, however, of LDLs are especially susceptible to oxidative damage by free radicals; damage to the lipid component may also ultimately result in damage to the protein component.  LDLs with damaged protein coats will not be recognized by the LDL receptors of cells.  These damaged LDLs, however, are phagocytized by macrophages through a different receptor, scavenger receptor A (Steinberg, 1997). The increased uptake of damaged LDLs results in vast quantities of cholesterol esters within the macrophage.  At this point the macrophage is known as a foam cell.  The strange accumulation of LDLs and foam cells within the walls of coronary arteries is the hallmark of cardiovascular disease.   The basic pathogenesis of atherosclerosis has been reviewed (Ross, 1993).

The study of cardiovascular disease (CVD) can be separated into:  1) mechanisms governing atherosclerosis and 2) mechanisms governing blood clotting.  Atherosclerosis is a degenerative disease of vascular endothelium.  The initiation of the atherogenic process may begin in response to injury of endothelial cells lining vessel walls.  This damage may result from a mechanical stress such as high blood pressure or from high levels of oxidized LDLs, which are known to be toxic to endothelial cells.  Monocytes, which differentiate into macrophages, and T-lymphocytes adhere to the damaged area as LDLs concurrently penetrate the endothelium and accumulate within the wall of the vessel.  Uptake of oxidized LDLs by macrophages is much greater than native LDLs (Steinberg, 1997).  Oxidized LDLs also trigger the release of cytokines by macrophages.  Cytokines play a pivotal role in mediating the atherogenic process through their chemotactic attraction of other white blood cells to the area.  As more LDLs enter the area they will become oxidized by HOOH and hypochlorite produced by the additional phagocytes.  A vicious cycle follows:  as more oxidative damage occurs to LDLs, more phagocytes are attracted to the area, and yet more damage occurs to LDLs.   The damaged LDLs are continually engulfed by macrophages via their scavenger receptor A.  The accumulation of foam cells and LDLs deep to the epithelium leads to occluded vessels and impeded blood flow.  The decreased speed of blood flow leads to pathological blood clotting which will cut off the blood supply to the tissue.  This commonly occurs in coronary vessels.  As the coronary vessels become blocked, the heart muscle becomes ischemic and death to the myocardium occurs; heart attack.

Studies on CVD cover a multitude of areas.  These areas include looking at platelet function and clotting, chemicals that affect vessel diameter and blood pressure, and plasma lipids and lipoproteins.  Numerous clinical and epidemiological studies have shown that these areas all appear to be influenced by dietary fatty acids (Krauss et al., 2000 and Simopoulos, 1999).  In general, it has been established that a diet high in saturated fatty acids (SFAs) shows a positive correlation with the risk of CVD because of hypercholesterolemic effects or unfavorable shifts in LDL:HDL ratios.  It has also been shown that the consumption of polyunsaturated fatty acids (PUFAs), provided that adjustments have been made for coconsumed SFAs, shows a negative correlation with CVD because of a hypocholesterolemic effect or favorable LDL:HDL shifts.  Eicosapentaenoic acid [EPA, 20:5(n-3)] and docosahexaenoic acid [DHA, 22:6(n-3)] are PUFAs found in fish oils which have protective effects against CVD (Mori et al., 1997).  3-series prostaglandins, which are antiaggregators and vasodilators, are derived from EPA and DHA.  It is possible, but unclear, that diets rich in these PUFAs exert their protective effects by lower blood pressure and decreasing platelet aggregation.  Another PUFA that decreases blood pressure is -linolenic acid [GLA, 18:3(n-6)].  GLA is quickly converted into a precursor for antiaggregator and vasodilator prostaglandins.  As previously mentioned, oxidized LDLs are strongly correlated with CVD.  Highly unsaturated fatty acids such as EPA, DHA, and GLA are highly susceptible to lipid peroxidation.  Circulating LDLs are protected from lipid peroxidation by antioxidants.  One of the major antioxidants is vitamin E, mainly -tocopherol.  It seems likely that dietary flavonoids (quercetin and catechin) contribute to the antioxidant defense and reduce the consumption of -tocopherol in both lipoproteins and membranes (Fremont et al., 1998). Because PUFAs are so susceptible to lipid peroxidation it could potentially increase the amount of damaged LDLs, thereby counteracting the beneficial effects of these PUFAs.  In 2001, Frenoux et al. published a study in the Journal of Nutrition that looked at whether a diet high in EPA, DHA, and GLA, known to exert antihypertensive effects, is associated with impaired antioxidant status.

Frenoux et al. used 20 spontaneously hypertensive rats (SHR) and 20 normotensive Westar Kyoto rats (WKY) as subjects.  The subjects were divided into four groups of 10, and were to be fed one of two diets, EPAX or Isio, for a 10 week period.  Both diets consisted of 5g/100g lipid content, however only one of the diets, the EPAX diet, contained significant amounts of GLA, EPA, and DHA.  Systolic blood pressures were established and blood samples were obtained.

Platelet aggregation values were determined.  Both the percentage of maximum platelet aggregation and the time to reach the value were obtained.  Plasma levels of -tocopherol, triacylglycerol, and total and free cholesterol concentration were determined.  Total antioxidant status was determined by RBCs ability to withstand free radical-induced hemolysis.  Impaired antioxidant status decreases the time 50% hemolysis (T50% hemolysis) is reached. The fatty acid composition of platelets and RBC membranes were also established.  Lastly, lipid peroxidation would be determined from the VLDL-LDL fraction.

At the end of the ten weeks, the SHR rats developed hypertension.  The SHR rats also had higher blood pressures than the WKY rats.  The SHR rats, however, fed the EPAX diet had significantly lower blood pressures than the SHR rats fed the Isio diet.  Because of previous findings by Engler et al and Narce et al, it was assumed that GLA, and not EPA and DHA, was primarily responsible for the decrease in blood pressure.  GLA is known to modify the renin-angiotensin-aldosterone mechanism and increase the production of a vasodilator prostaglandin.

Total antioxidant status was improved in SHR rats fed the EPAX diet and not the Isio diet.  This appears to be a direct contradiction with the fact that highly unsaturated fatty acids are susceptible to oxidation.  It was hypothesized by the experimenters, based on a study by Van Den Berg et al., that perhaps increased amounts of membrane PUFAs were oxidized, but that other membrane fatty acid oxidation was subsequently decreased.  The increased PUFAs in the membranes perhaps create an “oxidizable buffer”. This would then explain the overall higher total antioxidant status associated with the EPAX diet.  This is just one possible explanation for the increased antioxidant status.  It was also determined that both the SHR and WKY rats fed the EPAX diet had lower plasma total cholesterol levels.  Lower total cholesterol levels have been shown to decrease free radical production, and this could also explain the oxidative resistance in the EPAX fed SHR rats (Ohara et al.).

Overall, it appears a diet rich in GLA, EPA, and DHA produce  antihypertensive effects, increase resistance to lipid peroxidation, and lower plasma lipid concentrations.  These results do support that increasing these PUFAs in your diet may be a protective measure against developing CVD.


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