Thanks a lot for the post, Eric. I had a couple of questions for you if you don’t mind. You seem to be using fish oil and omega 3 PUFA interchangeably. I have read from several sources (Lyle’s site being one that you yourself referenced) that the real benefit is derived from the DHA. Humans are horrible at breaking omega 3 into EPA and subsequently converting to DHA (possible exception being in case of vegans). Do you attribute the positive effects from the supplementation to be from the DHA or would similar effects be seen in something like flax oil dosing? With all the new information on the importance of nutrient timing, would you advise consumption post workout or is there negligible benefit from that?
I’ll chime in here briefly. EPA and DHA have different roles in health, so it’s good to have enough of both.
I’m guessing what you are referring to with the poor conversion, is the conversion of the plant form of omega-3, alpha linolenic acid (ALA) in to the animal forms (EPA and DHA). If you do a search for some literature on this, humans are incredibly inefficient at this conversion process; we’re much better off letting algae and fish convert and concentrate the n-3s for us.
Thanks for the info. I actually was referring to EPA to DHA. I know that ALA to EPA/DHA is poor, but I have seen from a couple of sources that the majority of health benefits seem to be from the DHA than EPA (I would be interested in anything you have on the benefits of EPA).
Here is a link to an article Lyle wrote on the subject that details the poor conversion:
I think you raise two really important questions regarding the limitations of this research.
We’re absolutely on the same page when it comes to the benefits of DHA . And that’s an excellent piece you posted from Lyle — thanks!
Unfortunately, the authors of this study don’t propose any absolute molecular changes that subsequently augment the anabolic pathways. And no mention of whether EPA or DHA was more or less beneficial.
In fact, scientist are still hashing out just how n-3’s exert their effects at the cellular level (see the “GPR120 Study” that’s hyperlinked in the second paragraph). For these reasons, I really wouldn’t feel comfortable hypothesizing beyond what’s presented in the literature.
Regarding your question about nutrient timing, remember, these subjects were relatively untrained and were not asked to train throughout the 8-week experimental period. The increased pathway sensitivity leads me to believe that the effects were not through strategic nutrient timing, but rather some transient change to the cellular constituents.
Could there be some validity to n-3 nutrient timing (maybe through increased FAT/CD36 activity during training)? Maybe, maybe not. Clearly, more research is required to effectively answer these questions.
Very interesting. I wonder if the mTOR effects were more from EPA or DHA (or both had similar effects)? I also wonder if similar research has been done looking for similar effects from the base Omega 3 α-Linolenic acid?
In short, me too! I addressed some of your points in my answer to asomni — hope that helps.
One thing I will add is that the study was performed with high levels of both DHA and EPA. Considering the human body’s inefficient ALA conversion process, it might be safe to assume that things like flaxseed oil wouldn’t produce the same effect as another, more EPA/DHA potent n-3 supplement. That is, if the purported benefits are of direct result of the EPA/DHA supplementation and not overall n-3 concentrations.
Lyle’s said, ” … I don’t feel that ALA/flax oil is an appropriate EFA source.” I tend to agree here, BUT we need more research as to ALA’s effects pertaining to mTOR signaling to answer your question.
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