Let’s face it: fish oil is hip. Trendy. I see commercials on TV, every market has its own brand, and I hear the personal trainers at the gym recommending it to everyone they see.
But, despite that little part of me that wants to buck the trends and avoid health fads, I must face it: fish oil is actually good for you. Not just you though; it’s good for me, specifically.
I came to this realization as I was listening to a talk about diet-induced inflammation, and a curious case in which the mice under investigation seemed spared from the hyper-inflammatory state that was expected. The talk did not present a firm answer, but the suspected cause of the anti-inflammatory state was an increase in PUFAs.
Eh? PUFAs? Poly-unsaturated fatty acids. Fatty acids, as a general rule, are evil and inflammatory, and should be avoided given the oft-pronounced Obesity Epidemic. But certain fatty acids– namely, n-3 and n-9 PUFAs– actually block signaling from inflammatory immune receptors, resulting in less, rather than more, inflammation. Fish oil, as it turns out, is one of the most common dietary n-3 fatty acids (also known as omega-3 fatty acids).
Why is reducing inflammation important? Well, to begin with, rogue inflammation in adipose and muscle tissue is now seen as one of the primary causes of insulin resistance in type 2 diabetes. So, molecules and chemicals like the n-3 PUFAs that reduce inflammation have the potential to increase overall glucose sensitivity by reducing inflammatory signaling.
But, more importantly, since I’m talking about me here: type 1 diabetes is an autoimmune disorder. That means my immune system is leading an attack against its own cells and endogenous molecules. And that means my body is in a state of constant, low grade inflammation. The possibility that I could reduce that inflammation generally with a simple measure like taking a fish pill every morning, therefore, is attractive.
Now, to be clear: there is no guarantee here that n-3 PUFAs, which have a general anti-inflammatory profile, are always anti-inflammatory, or that in vivo (that is, in a living body) they have enough of an effect to overcome opposing signals. Further, there is no guarantee that a general anti-inflammatory profile has anything to do with my particular case of inflammation, which is complicated, specifically localized, and a result of a long-running series of adaptive and innate immune irregularities.
But, even without any assurance, I figure taking fish oil won’t hurt. Or rather, the chance that we will find out it has some horribly negative effect (or even some mildly negative effect) is much lower than the chance that it will do something noticeably good, which is lower still than the chance that it will either do something unnoticeable or do nothing at all.
In other words, sure– may as well.
And, maybe, just maybe, if I’m lucky, it will do something good internally. Like reduce inflammation just slightly, making things a bit easier for my body as a whole, or saving the last hidden vestiges of beta-cells that in my dreams I have. It’s not an unreasonable hope– in fact, a recent study published in Diabetes, “High Pancreatic n-3 Fatty Acids Prevent STZ-Induced Diabetes in Fat 1 Mice” , found that a particular transgenic mouse with a abnormally high ratio of n-3 to n-6 PUFAs was saved from beta-cell inflammation and ultimately ablation. The mice, which have a special gene from a roundworm, are especially prone to converting n-6 PUFAs to n-3 PUFAs, so even with the highly inflammatory diet they were fed, the transgenic mice maintained very high levels of n-3 PUFAs.
According to the researchers, these particular fatty acids helped to maintain normoglycemia and beta-cell mass in the mice after they were treated with streptozotocin (STZ), a toxin that induces a cell-killing inflammatory reaction within beta-cells. Levels of crucial inflammatory factors, including NFkB, were reduced, as were cytokines that perpetuate inflammatory signals and markers that indicate the inflammatory state of cells. At the same time, levels of n-3 fatty acids and related anti-inflammatory lipids were more abundant than in the wild-type counterpart mice.
The study lacks proof that the n-3 fatty acids rescued the mice from beta-cell death by directly reducing inflammation– in theory, the n-3 PUFAs could be blocking the action of STZ in some other way, meaning the lack of inflammation is secondary to the blocking of the toxin. Further, as the study notes, mice fed n-3 fatty acid-rich diets have in the past not been rescued from STZ-induced diabetes; the authors of the study speculate this has to do with the fact that the transgenic mice achieved a much higher ratio of n-3 to n-6 PUFAs than the mice in the dietary experiments, but this theory has yet to be tested. And then there’s the whole issue that even if n-3 PUFAs in pancreatic tissue help save mice from toxin-induced beta-cell apoptosis– well, my beta-cells went and apopted more than sixteen years ago now.
Still, those are small caveats in comparison to the growing body of evidence that shows n-3 PUFAs have potent anti-inflammatory effects, acting as dampeners on the NFkB party. So, considering the low monetary and temporal cost of adding PUFAs to my diet, the answer for me at least is clear: time to start popping fish pills!
 Bellenger J, Bellenger S, Bataille A, Massey KA, Nicolaou A, Rialland M, Tessier C, Kang JX, Narce M. High Pancreatic n-3 Fatty Acids Prevent STZ-Induced Diabetes in Fat-1 Mice: Inflammatory Pathway Inhibition. Diabetes. 2011 Feb 17. http://www.ncbi.nlm.nih.gov/pubmed/21330635