Are statins and omega-3s incompatible?

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)
--Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)
--Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.

Comments (4) -

  • Ellen Lewis

    6/18/2013 7:32:42 PM |

    thanks, this seems a sensible take on the issue.

  • Dolph

    6/30/2013 4:59:57 PM |

    This is a (too) far stretched conclusion pretty obviously. O3s still haven’t shown any consistent benefit alone, with a statin drug or without it, and cherry picking the studies that seem to look doesn’t help that fact either! The data is just inconclusive.

    A much more interesting blog article I hope to read in the future would be about niacin!
    Niacin has shown more than once to produce favourable outcomes alone and combined with resins. (CDP, FATS, etc.) On the other hand there can be no more doubt that it doesn’t add any benefit to statin therapy after the results of the two big clinical endpoint studies (AIM-HIGH and HPS2-THRIVE), that flush the cute little landmark studies (ARBITER, HATS, etc.) down the toilet where they belong.
    So what does that imply for the TYP-programm? A rhetorical question it should be, but I’m sure somebody will add some woo…

    - See more at:

  • Stephen in Jacksonville

    7/3/2013 10:15:53 PM |

    It is interesting that he should be doing this research into how statins react with Omega-3's. Statins may be one of the most widely prescribed drugs at this point, and I certainly think more research should be conducted on their long-term effects. I recently read about another study which looked at the effects of exercise and statins. Apparently, this drug actually works to counteract some of the benefits that are gained by getting regular exercise for people with cholesterol problems.

  • Brandon Barclow

    7/18/2013 6:07:47 PM |

    Stephen in Jacksonville.   There's no maybe to it.  The number 1 and number 2 selling drug in the world are statin drugs.  32 million Americans are currently taking statin medication.  The one thing that the 32 million have in common is:  THEY HATE TAKING THEIR MEDICATION.

Heart Scan Curiosities #7

Heart Scan Curiosities #7

Here's a situation that crops up once in a while, occurring in perhaps 2% of heart scans.

The white within the circled area represents calcium, and thereby atherosclerotic plaque, situated immediately at the "mouth", or opening, of the the right coronary artery. What is somewhat unusual is that this plaque is not principally coronary, but aortic. That is, the plaque is mostly situated in the large vessel called the aorta. The three coronary arteries arise from the aorta.

In this instance, the aortic plaque involves the mouth of the right coronary artery. (In views not shown, the plaque also extends into the artery as well.) I call this a "double whammy" because the same plaque can post risk for heart attack and stroke.

Generally, aortic plaques pose risk for stroke. When aortic plaque fragments, little bits and pieces can travel upward to the brain and block an artery, thus a stroke.

In the coronaries, disrupted ("ruptured") plaques don't generally shower debris, but permit blood clot formation, resulting in heart attack.

This plaque, however, poses the theoretical risk of both heart attack and stroke because of its strategic location.

Should a plaque like this be handled any differently? I don't think so. But it does provide another reason to take atherosclerotic plaque in any artery seriously.

Comments (1) -

  • Anonymous

    11/12/2008 5:12:00 AM |

    I just had my first heart scan at Boulder, CO.  My heart scan score was zero, but my descending aorta showed as mildly calcified.

    I wonder what conditions determine whether plaque builds up in the coronary arteries versus in the aorta.  

    And I also wonder how mildly calcified would score if it was in the coronary arteries rather than in the aorta.  I know how to interpret the zero heart scan score, but I don't know how to interpret the mildly calcified aorta.  Since it is in the descending aorta, I believe it is less dangerous than the case discussed here.