In the 1970s researchers found that the Greenland Inuits had much less heart disease than Westerners. The researchers examined the Inuits’ diet to try to find out if diet had anything to do with it. The Inuits’ diet had a higher potassium sodium ratio than the usual Western diet. And it had a higher percentage of polyunsaturated fats (PUFAs) from the large amount of fish the Inuits ate. This finding led to more research to determine whether polyunsaturated fats protected against heart disease, and whether omega-3 fats protected better than omega-6 fats.
DHA And EPA
Two main omega-3 fatty acids were found to be cardioprotective. These were DHA and EPA. They both had similar protective effects on some of the cardiac markers found in blood. For example, DHA and EPA have similar effects on lowering triglycerides in blood tests. Triglycerides are part of the blood tests performed to determine future risk of heart attack. Because of this and other effects that are felt to be cardioprotective, DHA and EPA are often studied together for other possible ways of protecting the heart.
A recent article (1) examined if DHA and EPA protect the heart cells directly. They tried to find out if DHA and EPA protected against heart failure by preventing the death of heart muscle cells that occurs when their mitochondria (the cell power plants) stop working.
DHA And EPA Reduce Inflammation
In this study the researchers gave DHA and EPA together in the diet. They found that the mitochondrial membranes in heart muscle cells replaced arachidonic acid (AA) with DHA and EPA. This is important because AA can cause an inflammatory response when a cell bursts and dies, leading to scar tissue.
Replacing AA with another fat should lead to less inflammation if a cell bursts. In the heart, less inflammation means less scarring and less heart failure.
Which Is Better – DHA Or EPA?
To find out if both DHA and EPA were equal, or if one was better than the other, the researchers fed these two omega-3 fatty acids separately. They gave DHA by itself and EPA by itself. They found that DHA by itself increased both DHA and EPA in the mitochondrial membranes, and lowered arachidonic acid. So DHA by itself should lower inflammation and scarring.
When EPA was given by itself it increased EPA in the mitochondrial membranes, but not DHA. And it did not lower AA as much as DHA did. So EPA was less effective at preventing inflammation and scarring.
The researchers also studied whether DHA and EPA could prevent the heart muscle cell death involved in heart failure. If the cells do not die they won’t release AA. There will be no scarring. And the heart muscle cells will remain alive to continue strengthening the heart.
Heart muscle cell death results from activation of mPTP channels in mitochondrial membranes. DHA by itself hindered the mPTP channel, stopping cell death and subsequent scarring. This should result in less heart failure.
When EPA was given by itself it did not hinder mPTP. The mitochondria swelled and the cells died. Because EPA did not prevent heart cell death, it should not protect against heart failure as much as DHA.
As discussed in a previous posts, DHA appears to protect against heart failure and the early effects of hypertension from a poor potassium sodium ratio. This study showed how DHA does this. The mechanism for this protection appears to be DHA’s action on preventing cell death, and reducing potential inflammation in the heart.
This does not appear to be the case, however, for EPA. EPA does not prevent heart muscle cell death, but does reduce inflammation when heart muscle cells die. It just does not reduce inflammation as much as DHA.
No Ester, Please
DHA needs to be in the form found in fish to provide these effects, though. As discussed here, DHA as an ethyl ester (the form often found in capsules) does not protect against heart disease.
1. Dietary supplementation with docosahexaenoic acid, but not eicosapentaenoic acid, dramatically alters cardiac mitochondrial phospholipid fatty acid composition and prevents permeability transition. Khairallah RJ, Sparagna GC, Khanna N, O’Shea KM, Hecker PA, Kristian T, Fiskum G, Des Rosiers C, Polster BM, Stanley WC. Biochim Biophys Acta. 2010 Aug;1797(8):1555-62. doi: 10.1016/j.bbabio.2010.05.007. Epub 2010 May 21.