It appears that the evolutionarily unprecedented high omega-6 and low omega-3 intake in the modern western diet causes excessive series-2 prostaglandin and thromboxane (TXA2) formation, and resulting inflammation and cardiovascular effects- and low dose aspirin is an attempt to combat this. Why not fix the problem at it’s source?
Reducing omega-6 oils in your diet and increasing omega-3 should have a similar effect, but with more proven safety and effectiveness: nearly all humans did this until industrial seed oils became popular in the last few decades (see this video series from biochemist Dr. Bill Lands for more details http://youtu.be/dgU3cNppzO0 ).
Aspirin works primarily by suppressing production of thromboxane and inflammatory series-2 prostaglandins from omega-6 fats, by inactivating the cyclooxygenase enzymes (COX-1, and COX-2). Omega-3 fats also competitively inhibit this same enzyme, by competing with omega-6 fats to be metabolized into less inflammatory series-1 and series-3 prostaglandins.
There are other important benefits of fixing the omega 3⁄6 ratio in your diet as well- their ratio is reflected in tissue lipid membranes, and likely influences the proper function of these membranes. Continuing on a high omega-6 diet and trying to counter-act this with aspirin seems less than ideal.
It would be interesting to see some data showing the effectiveness of low dose aspirin in countries that already have a healthy omega 3⁄6 ratio (such as Greenland or Japan). I would be very surprised if it still has the same benefit in such a group.
As a person who has a nearly 1⁄1 omega-6 to long chain omega-3 ratio in my diet (I regularly eat fatty cold water fish and avoid seed oils), I wouldn’t consider low dose aspirin to be a prudent risk adverse decision unless I saw data showing it’s benefits reproduced in others with a similar intake ratio.
I retracted this, because I have learned a lot more about this issue in the last year. I am still undecided on aspirin, however I no longer think that the mechanisms mentioned above are the only important roles aspirin plays. I am also no longer convinced that omega-3 offers a health benefit, and that omega-6 restriction alone may be superior to replacing omega-6 with omega-3.
If you look at the Rothwell paper linked above by gwern, there’s one Japanese study there—JPAD (Ogawa H, Nakayama M, Morimoto T, et al. Japanese Primary
Prevention of Atherosclerosis With Aspirin for Diabetes (JPAD)
Trial Investigators. Low-dose aspirin for primary prevention of
atherosclerotic events in patients with type 2 diabetes:
a randomized controlled trial. JAMA 2008; 300: 2134–41).
Looking at the graphs, JPAD effectively showed zero effect of aspirin. I think this supports your thesis.
But from JPAD, the specific effects that are supposed to show aspirin benefits weren’t what this study measured! They were looking at:
Primary end points were atherosclerotic events, including fatal or nonfatal ischemic heart disease, fatal or nonfatal stroke, and peripheral arterial disease.
This doesn’t include anything related to cancer. And to the extent that the study did look at all-cause mortality, it showed exactly what you would expect from a relatively small (n=2539) and short (“median follow-up of 4.37 years”) trial where aspirin was yielding benefits: a large but non-statistically-significant effect
A total of 34 patients in the aspirin group and 38 patients in the nonaspirin group died from any cause (HR, 0.90; 95% CI, 0.57-1.14; log-rank test, p=.67).
I haven’t looked at the JPAD paper yet, but that Cochrane study plots JPAD results for cancer endpoints as well as major vascular and extracranial bleeds. In the same graphs I don’t see large effects.
It’s worth pointing out the general low cancer rates (in the controls as well) in the JPAD study.
It appears that the evolutionarily unprecedented high omega-6 and low omega-3 intake in the modern western diet causes excessive series-2 prostaglandin and thromboxane (TXA2) formation, and resulting inflammation and cardiovascular effects- and low dose aspirin is an attempt to combat this. Why not fix the problem at it’s source?
Reducing omega-6 oils in your diet and increasing omega-3 should have a similar effect, but with more proven safety and effectiveness: nearly all humans did this until industrial seed oils became popular in the last few decades (see this video series from biochemist Dr. Bill Lands for more details http://youtu.be/dgU3cNppzO0 ).
Aspirin works primarily by suppressing production of thromboxane and inflammatory series-2 prostaglandins from omega-6 fats, by inactivating the cyclooxygenase enzymes (COX-1, and COX-2). Omega-3 fats also competitively inhibit this same enzyme, by competing with omega-6 fats to be metabolized into less inflammatory series-1 and series-3 prostaglandins.
There are other important benefits of fixing the omega 3⁄6 ratio in your diet as well- their ratio is reflected in tissue lipid membranes, and likely influences the proper function of these membranes. Continuing on a high omega-6 diet and trying to counter-act this with aspirin seems less than ideal.
It would be interesting to see some data showing the effectiveness of low dose aspirin in countries that already have a healthy omega 3⁄6 ratio (such as Greenland or Japan). I would be very surprised if it still has the same benefit in such a group.
As a person who has a nearly 1⁄1 omega-6 to long chain omega-3 ratio in my diet (I regularly eat fatty cold water fish and avoid seed oils), I wouldn’t consider low dose aspirin to be a prudent risk adverse decision unless I saw data showing it’s benefits reproduced in others with a similar intake ratio.
I retracted this, because I have learned a lot more about this issue in the last year. I am still undecided on aspirin, however I no longer think that the mechanisms mentioned above are the only important roles aspirin plays. I am also no longer convinced that omega-3 offers a health benefit, and that omega-6 restriction alone may be superior to replacing omega-6 with omega-3.
If you look at the Rothwell paper linked above by gwern, there’s one Japanese study there—JPAD (Ogawa H, Nakayama M, Morimoto T, et al. Japanese Primary Prevention of Atherosclerosis With Aspirin for Diabetes (JPAD) Trial Investigators. Low-dose aspirin for primary prevention of atherosclerotic events in patients with type 2 diabetes: a randomized controlled trial. JAMA 2008; 300: 2134–41).
Looking at the graphs, JPAD effectively showed zero effect of aspirin. I think this supports your thesis.
But from JPAD, the specific effects that are supposed to show aspirin benefits weren’t what this study measured! They were looking at:
This doesn’t include anything related to cancer. And to the extent that the study did look at all-cause mortality, it showed exactly what you would expect from a relatively small (n=2539) and short (“median follow-up of 4.37 years”) trial where aspirin was yielding benefits: a large but non-statistically-significant effect
I haven’t looked at the JPAD paper yet, but that Cochrane study plots JPAD results for cancer endpoints as well as major vascular and extracranial bleeds. In the same graphs I don’t see large effects.
It’s worth pointing out the general low cancer rates (in the controls as well) in the JPAD study.