Leaning Out on a Bulk? Approx. 6g of Phospholipid(!)-Bound DHA + EPA Per Day Could Make That Possible. Rodent Study Reveals Profound Difference to "Regular Fish Oil"

Can phospholipid-bound N-3s as in krill ward off the fat gain on a bulk?

Your daily visits, comments, feedback, criticism and obviously commendations are not only what makes the hours of work I invest into this blog worthwhile, they are also a constant source of "inspiration" and, as the latest post by Roy Nelson on the SuppVersity Facebook Wall goes to show you, oftentimes point me towards the most interesting stuff. In that, it does not really matter that Roy's question was more or less unrelated to what I personally found absolutely newsworthy in the study he referenced, a study which deals with fish oil supplementation and its *yawn* anti-inflammatory effects.

You learn from me, I learn from you

Now, I guess some of you are similarly fed up with those rodent studies like I am, but bear with me folks, Roy did in fact shoot the bulls-eye with this one (not sure if you realized that Roy, but you did ;-) After all, there was a certain twist to this study. A twist you have actually read about on the suppversity roughly 7 month ago, in a post with the suggestive title "Phospholipid or Triglyceride? What's in Your Fish Oil Caps? Only Phospholipid Based DHA+EPA Reduces Fat Cell Growth & Elevated Insulin Levels Despite Obesogenic Diet" (read more). Both studies, the one at hand, which was published only a couple of days ago in Nutrition & Metabolism, as well as the "old" study by Rossmeisel et al. (read up on the results), dealt with the difference between the "real-rodent-world" differences between triglyceride and phospholipid based n3-PUFAs.

Why are you talking about "n-3 PUFAs" and not simply about fish oil? There are actually two reasons, I am trying to avoid the term "fish oil" in this context. Firstly, real fish has both, triglycerides which make up >90% of the fat in fatty fish like salmon & co. And secondly, the way fish oil supplements are produced usually removes the last phospholipid fractions leaving you with nothing but the triglycerides (another reason to stick to fish as an animal, instead of fish as a gelatine cap ;-)

Rossmeisel et al. have already been able to show that the phospholipid-bound n-3 PUFAs (DHA and EPA) posses physiological effects the cheap triglycerides don't have to offer: They decrease the size of the fat cells and thus provide a structural advantage, the common triglyceride-bound forms of DHA and EPA do not have to offer.

Why is a smaller adipocyte size significant?

Remember the post on choline as part of a weight loss stack (read more)? Guess what: Choline is also part of most phospholipids.

I have been dabbling with adipocyte sizes in previous posts and freely admit that this is a too complex matter to actually support the statement that "small adipocytes are best" (learn more in previous posts).

In a hypercaloric diet scenario, as the one in the study at hand, a  decreased adipocyte size may yet well be considered the structural foundation of reduced baseline inflammation. after all, the size or you could as well say the filling level o the fat cells is directly associated with the amounts of pro-inflammatory cytokines they release (Skurk. 2007).

For those of you who are in fact dabbling with high levels of fat-induced inflammation (these are often the skinny fat guys and girls), this alone would therefore warrant the investment in Krill instead of fish oil, if you can't or don't want to get your dietary phospholipids from fresh fish. The new findings the study by Manar Awada and his (or her?) colleagues from the CarMeN Laboratory in Lyon, France, brings to the table are yet probably a more convincing argument for the majority of physical culturists:

Phospholipid-base N3-PUFAs reduce will cut body fat even on a HFD diet

Yep, that's right. If the results of the Awada study translate 1:1 from you rodents to physical culturists, you could in fact up your caloric intake by 50% and still lose 14% body fat compared to following a "species-appropiate diet" (in the case of a rodent that's obviously a high carb diet, with a macronutrient ratio of 19.1% protein, 57.6 carbohydrates and12.8% fat in it).

Figure 1: Energy intake and body composition (left) and lipid, glucose, insulin and leptin levels (right); data expressed relative to values from the regular low-fat chow group (Awada. 2013)

Now the data in figure 1 and the notion that you could cut body fat on a bulk certainly sounds too good to be true and to be honest, I have my doubts that someone whose following all the nutritional advice you get on the SuppVersity on an almost daily basis will see identical "real-human-world" results (specifically if your diet already contents phospholipid bound N3-PUFAs, which it will if you follow my advice to have fish once or twice a week). But let's be honest, if the consumption of phospholipid bound DHA and EPA at a dosage of 0.08g/kg body weight did nothing but blunt the almost inevitable fat gain on an intense (+50% increase in energy intake) "bulk", that would be awesome - wouldn't it?

What are the underlying mechanisms, here?

Krill protein offers non-negligible health benefits, as well (learn more).

I know many of you mainly interested in the practical implications, but especially, when we are dealing with data from rodent studies, we have to understand how a supplement works, in order to tell something about the probability that it will work in humans as well.

Against that background, it's well-worth to take a final look at those cellular parameters that may provide some clues on what it is that makes the phospholipid forms of DHA and EPA so superior compared to their conventional triglyceride counterparts.

Aside from a highly more pronounced increase in intra-cellular vitamin E (2.8x higher than HFD alone and 1.5x higher than HFD + triglyceride-bound omega-3s), there were yet unfortunately no statistically significant inter-group differences. Even in conjunction with the (probably related) yet statistically non-significant difference in markers of lipid peroxidation (4HHE 104, 89, 128nM and 4HNE 13, 6, 9nM in high fat, high fat + PL and high fat + TG, respectively), this is simply not enough to gain insight into the underlying mechanisms which lead to these highly desirable anti-obesity effects. So that we will, for better or worse, have to contend ourselves with the scientists' own conclusion that "further research is required to better understand the mechanism of action of PL carrier".

Figure 2: The PL N-3 content (g/100g dry mass) of fish is very heat stable compared to the triglyceride fraction of which are partly (baking) or totally (frying) lost when you process the raw fillets (Mai. 1978). So even if your fish has a relatively low PL content, that will at least remain where it is supposed to be ;-)

Bottom line: Without knowing the underyling mechanism and in the absence of respective human data, I am honestly hesitant to suggest you go and buy tons of krill oil supplements. After all, the human equivalent dosage of the amount of phospholipid bound DHA+EPA that was used in the study at hand amounts to ~6g per day. So even if found a product that's 100% phospholipid, 0% triglyceride you would have to take ~30 1g caps of regular krill oil which usually have ~200mg of DHA and EPA in them.

So unless you happen to have a cheap source of the purified omega-3 phospholipids the scientists used in their study, it will probably be more prudent to wait for the third SuppVersity post on this matter and invest the buckloads of money this will save you into fresh fish fillets. 

References:

• Awada M, Meynier A, Soulage CO, Hadji L, Géloën A, Viau M, Ribourg L, Benoit B, Debard C, Guichardant M, Lagarde M, Genot C, Michalski MC. n-3 PUFA added to high-fat diets affect differently adiposity and inflammation when carried by phospholipids or triacylglycerols in mice. Nutr Metab (Lond). 2013 Feb 15;10(1):23.
• Mai J, Shimp J, Weihrauch J, Kinsella JE. Lipids Of Fish Fillets: Changes Following Cooking By Different Methods. Journal Of Food Science. 1978; 43: 1669–1674.
• Skurk T, Alberti-Huber C, Herder C, Hauner H. Relationship between adipocyte size and adipokine expression and secretion. J Clin Endocrinol Metab. 2007 Mar;92(3):1023-33.