Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 15 No. 4 • August 2012


Effects of Different Ratios of Omega 6/Omega 3
Polyunsaturated Fatty Acids on Infarct Size
After a Heart Attack in Rats

Researchers hypothesized, on the basis that dietary omega-6 fatty acids and omega-3 fatty acids could modulate the balance between pro- and anti-inflammatory mechanisms, that a decrease in the ratio of omega-6/omega-3 (that is, an increase in omega-3 fatty acids as compared to omega-6 fatty acids) in the diet, without altering the content in total fat, proteins, or carbohydrates, would result in a reduction in infarct size (the amount of heart tissue killed) in a myocardial infarction (MI).1 They also hypothesized that the decreased omega-6/omega-3 in the diet would diminish the apoptosis (cell death) that occurred in the amygdala and hippocampus of the brain following reperfusion (restoration of blood flow) after the MI.

Three month old male Sprague Dawley rats were fed diets with one of three possible ratios of omega-6/omega-3 fatty acids for two weeks: 1:5, 1:1, or 5:1.

After that, the researchers induced myocardial infarction (heart attack) in the animals while the animals were under anesthesia by occluding the left anterior descending coronary artery; then, after 40 minutes of ischemia, there was 15 minutes of reperfusion, after which the animals were killed and heart and brain tissues prepared for examination.

Infarct size was significantly reduced by 32% in groups 1:5 and 1:1 as compared to group 5:1 omega6/omega3 ratios. The plasma levels of the proinflammatory cytokine TNF-alpha (tumor necrosis factor alpha), released following myocardial infarction (MI) was significantly increased in the 5:1 diet group as compared to the two other groups. Various brain areas were examined—the dentate gyrus, areas CA1 and CA3 and the lateral and medial amygdala—with particular attention paid to the limbic system where damage following an MI (from reduced blood flow and the release of inflammatory cytokines) is thought to be a causative factor in the depression that often follows an MI. In fact, after 15 minutes of reperfusion, caspase-3 activity (a mediator of apoptosis) was significantly reduced in the groups receiving high omega-3 polyunsaturated diets (1:1 and 1:5).

The researchers, taking all the results into consideration, concluded that “the 1:1 ratio is optimal for heart health.” (This conclusion, though, was derived from the parameters measured following MI in their 3 month old male Sprague Dawley rats, not from a study of heart health in general.)

The authors add, as a potential explanation of some of the results, that the omega-3 polyunsaturated fatty acids have antiapoptotic effects. For example, docosahexaenoic acid (DHA) is precursor for the antiinflammatory neuroprotectin D and systemic DHA administration after middle cerebral artery occlusion has been reported to increase levels of circulating neuroprotectin D. Interestingly, neuroprotectin D1 has been identified as an inhibitor, at very low doses, of inflammatory pain.2 In fact, the DHA derived NPD1 was first identified in resolving inflammatory exudates in mouse brain, as well as in experimental stroke, where it was found to provide potent protective actions (neuroprotection).2

In another study,3 human subjects that had lower levels of DHA in red blood cells (those in the lowest quartile when compared to those in higher quartiles) had significantly smaller brain volumes and also had significantly lower scores on tests of visual memory, executive function, and abstract thinking.3

An earlier study4 reported that a marker of inflammation (hs-CRP, high sensitivity assay C-reactive protein) was modestly but significantly elevated in autopsy samples from patients dying suddenly with severe coronary artery disease and that the association of hs-CRP with sudden death in heart disease patients was independent of age, smoking, and body mass index.

Actually, we don’t know anybody (including ourselves) who eats a diet (or even a diet plus supplementation) so enriched in omega-3 fatty acids as to reach a 1:5, let alone a 1:1 ratio. But the results of this study suggest that, if a heart attack is going to take place, you are going to be a lot better off if you have an omega-6/omega-3 ratio that is better (that is, lower) than the typical 16:1 in the average North American’s diet.1

References

  1. Rondeau et al. Effects of different dietary omega-6/3 polyunsaturated fatty acid ratios on infarct size and the limbic system after myocardial infarction. Can J Physiol Pharmacol 89:169-76 (2011).
  2. Park et al. Resolving TRPV1- and TNF-alpha-mediated spinal cord synaptic plasticity and inflammatory pain with neuroprotectin D1. J Neurosci 31(42):15072-85 (2011).
  3. Tan et al. Red blood cell omega-3 fatty acid levels and markers of accelerated brain aging. Neurology 78:658-64 (2012).
  4. Burke et al. Elevated C-reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies. Circulation 105:2019-23 (2002).

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