Sesame Powered High Omega-6 Diet Boosts Endurance Performance in Rodents - High Omega-3 Diet Sucks: Intra-Muscular Lipid Ratios Determine Exercise Performance

At least in rodents omega-6s appear to make abetter match with exercise than in human beings.

I actually referenced this study several times in the past. It came up in a Facebook conversation I had with Roy Nelson who pointed me to a press release telling me that (I quote) "Certain Fat Could Help Humans Lose Weight". Interestingly, the "certain fat" in this particular study is (brace yourselves) linolic acid, better known as "omega-6" (obviously a misnomer, since omega-6 is actually referring to a whole class of fatty acids).

In view of the fact that the corresponding study in which Rogowski et al. observed a significant correlation between the omega-6 fatty acid content in the muscle and mitochondrial uncoupling and fat oxidation. The problem with the study is however that it was conducted not just with mice, but with genetically modified mice.

The results of the said study by Rogoswki, Patin et al. may thus form the basis for further investigations, but should not be taken as "hard evidence" that a high intake of omega-6 fatty acids will have similar effects. The accumulation of linolic acid in the mouse muscles was after all a result of the genetic modification and not the consequence of high n-6 chow.

So what's the effect of dietary linolic acid, then?

Unlike Rogowski et al., Kerry J. Ayre and A.J. Hulbert from the University of Wollongong did not just use normal male Wistar rats as their test objects, they also did what the scientists from Texas Tech didn't do: They supplied their rodents with diets with different fatty acid profiles.

Table 1: If you have ever wondered about the "evolution" of the omega-3 vs. omega-6 ratio in our (=the human) diet, I suggest you take a closer look at the table to the right. According to this overview from a 2004 paper by Artemsis Simopoulus in Food Reviews International. As you will see, it has more than just reversed ever since the paleolithic era.

All diets contained the exact same macronutrient composition with 22%, 56% and 22% of the total energy being derived from fat, carbohydrates, and protein, respectively. The amount of essential fatty acids and their ratios in the 22% fat content of the diet did however differ significantly:

• 

  Irrespective of the fact that it sucks for rodent endurance, coconut oil could help you approach a flat tummy like the one above| learn more

  Coconut diet: Designed as (almost) "essentially fatty acid free", the coconut oil based diet had a saturated fatty acid / mono-unsaturated fatty acid / N-6 / N-3 ratio of 95:4:1:0
• High N-6: Being based on sesame oil, the high N-6 diet had a SFA / MUFA / N-6 / N-3 ratio of 16:30:50:4 that translates to an N-3:N-6 Ratio of 0.08 (1:12.5); now that sounds crazily low, but the average Westerner consumes a diet with a N-3:N-6 ratio of 0.0625 (1:16; cf. Simpopoulos. 2004) in other words - that was not even "as bad" (?) as the Western diet
• High N-3: By adding both sesame and a commercially available omega-3 supplement to the diet, the scientists hit a 21:25:35:16 ratio for SFA / MUFA / N-6 / N-3 - that's still far from "N-3 exclusive" but much more like what current expert advice tells us we should strive for, i.e. 1g of omega-3 for every 2g of omega-6

If we go by the contemporarily popular dietary paradigms, it should be obvious that the health of the rodents in the N-6 diet will take a beating. Against that background it is all the more surprising that it were the rodents in the high N-6 group that outdistanced their hairy competition in an endurance test at the end of the 9 week study period.

Figure 1: Fatty acid composition of the diets and corresponding endurance performance of male Wistar rats after 9-weeks on coconut, high n-6 and high n-3 diet (Ayre. 1997)

What's more, it's not as if the omega-6 mice had simply been running slower and were thus able to run for a longer time, they did also have higher workloads (=product of body mass, distance traveled, and percentage grade of the incline).

"So where is the connection to the new study from Texas Tech, then?"

If we look back at the initially mentioned results from the Texas Tech study, it appears logical to assume that the beneficial effects on the endurance capacity could be another downstream effects of an increased ability to oxidize dietary fats (which is basically what the Rogowski, Paton et al. argued). Compared to the minimal amount of blood glucose and the highly limited glycogen stores in the muscle and liver, the fat stores of mice (and man) do after all hold an almost inexhaustible amount of energy - they just have to be accessed.

Figure 2: Skeletal muscle fatty acid composition after 9 weeks (Ayre. 1997)

As you can see, in figure 2 the fatty acid composition of the skeletal muscle of the rodents in the Ayre study did reflect the fatty acid composition of the diets (remember: the changes in the Rogowski study occured on the same chow, simply due to a genetic mutation) and the significantly increased omega-6 content in the N-6 group mirrors the effect Rogowski et al. observed in response to their neat GMO tricks. It does therefore appear logical to assume that the rodents in the Ayre study experienced a similar upregulation of PPAR-delta (unfortunately back in the day scientists did not measure that). The latter would increase the oxidation of fatty acid and thus the energy availability during aerobic activity.

"Making the Right Fish Choices" is important for your healths, so I suggest you learn how in the same-titled SuppVersity article.

What should not go unmentioned is that the performance discrepancies were very long-lived. Even after 5 weeks on a regular diet, the rodents in the N-6 diet easily outperformed their coconut and omega-3 competition - probably because it takes months (in rodents and years in men) to restore a "normal" muscular fatty acid profile. Now this is an interesting thought, because it will eventually lead us to the hypothesis that the huge benefits we are currently seeing (at least in some individuals) from the consumption of supplemental omega-3 fatty acids would be a direct result of the their effect on a cellular fatty acid ratio that has been messed up over years!

In view of the profundity of the omega-6 overshoot in the SAD diet and considering the fact that many of us have been consuming diets containing 15x more omega-6 fatty acids than omega-3s for decades, this does not appear unlikely. From a scientific perspective it would yet reaffirm that the "optimal n3:n:6 ratio" for someone with a well-balanced cellular level of the latter could be very different from the 1:1 optimum some experts currently recommend as target in the battle against diabesity - right?

Swine study says 1:5 ratio of N3:N6 or higher = optimal health | more

Let's ground ourselves: Don't take this post as an incentive to guzzle vegetable oil all day.

As a strength athlete you may actually harm yourself as it appears that the high omega-6 intake favors the oxidative over the glycolytic pathway. As an endurance athlete, however you may reconsider how important it really is for you to avoid all omega-6 fatty acids as a plague.

On a more general note, it may in fact be worth to take another look at "optimal ratios". While some of the effects of the polyunsaturated fatty acids are in fact acute, their major effects appear to be brought about by their accumulation in our bodies.

The "optimal intake" will thus necessarily depend on the status quo, i.e. the current tissue level of n-3 and n-6 fatty acids and their respective ratios. Against that background we should not be surprised that you can counter the negative effects of an imbalanced diet by administering another imbalanced diet. In our case this is a correction of a profound omega-6 overshoot that can be achieved by increasing our consumption of omega-3 rich foods and limiting our use of omega-6 laden vegetable oils and the products of which the "food" industry tells us they were good for us, because they contain only healthy vegetable oils... this is a practice I have recommended in the past and something I still recommend today.

What I would hope we could agree on, though is the idea that the study at hand, despite being conducted in rodents should remind us that simply switching from one scapegoat to another did not help us, when that scapegoat was saturated fat. Do you really believe the outcomes will be better, when we simply glue the "avoid like a plague" sticker to the omega-6s? Yes? Well, I guess the first thing you should do then, is take your beloved extra-virgin olive oil and pour it away! Why? Well, 10% omega-6 and basically no omega-3 - that's a no go ;-)

References:

• Ayre KJ, Hulbert AJ. Dietary fatty acid profile affects endurance in rats. Lipids. 1997 Dec;32(12):1265-70. 
• Pella D, Dubnov G, Singh RB, Sharma R, Berry EM, Manor O. Effects of an Indo-Mediterranean diet on the omega-6/omega-3 ratio in patients at high risk of coronary artery disease: the Indian paradox. World Rev Nutr Diet. 2003;92:74-80.
• Rogowski MP, Flowers MT, Stamatikos AD, Ntambi JM, Paton CM. SCD1 activity in muscle increases triglyceride PUFA content, exercise capacity, and PPARδ expression in mice. J Lipid Res. 2013 Oct;54(10):2636-46.
• Simopoulos, AP. Omega-6/omega-3 essential fatty acid ratio and chronic diseases. Food Reviews International. 2004; 20(1).

Devil in the Feeding Trough: PGE-Response to "Bad" Red Meat from Grass-Fed Cattle Could Prevent not Cause Cancer, Stroke and a Whole Host of Autoimmune Diseases.

Image 1: You do not need to hunt your red meat like a paleolithic human being, just make sure it comes from grass-fed animals and you will have a "health food" that modulate the your prostaglandin response to inflammatory assaults and thusly reduce your risk of cancer, stroke and autoimmune disesases in a way no fat-free chicken breast will ever do.

I have had this in the news before, in the context of the purported health benefits of CLA, with respect to the modulation of the n3/n6 ratio in your diet and in various other context, you heard me saying, or, I should say, read me writing that rather than popping tons of fish oil caps, you should rather focus on decreasing your overall omega-6 intake by making healthy food choices at the supermarket. In this regard, choosing grass-fed over commercially raised beef (and other meat) products could turn out to be one of the most far-reaching choices you can make. While that alone will help you to concomitantly reduce the n-6 overload, as well as the overall PUFA-burden that is so characteristic of the "Western diet", a recent study shows that eating red meat, even instead of the "healthy" white fat-free chicken breasts, everyone is pounding these days, could actually have profoundly beneficial effects on your (auto-)immune health, protect you from cardivascular disease and (this is important for the ladies) get your menstrual periods and related issues back in order.

How grass-fed beef can help and why it outperforms bison, elk and chicken

In their study, the results of which were published in issue 31 of the journal Nutrition Research, K. Shane Broughton, Daniel C. Rule and Eldon Handrich did what scientists have been doing for decades now. They took mice (your usual carnivorous animal) and put them on one of those grain-based diets that was then enriched with "bad" red meat to make the animals sick. Well, ... while the design was in fact the same, the good news is that the intention was by way of exception not to show "prove" (as if mainstream dietary advice would be interested in "proof", anyway) how bad those nasty red meats are, but to evaluate whether the

[...] consumption of meat from range-fed bison vs range-fed and grain-finished cattle and grain-finished bison would lead to reductions in PGE-2 [prostaglandin E2] release without altering PGI-2 [prostacyclin] release after an infl ammatory stimulus in a mouse model.

Or put simply, the scienists wanted to check whether there was any truth to the superiority of bison compared to the "bad" red meat, when it comes to balancing out the ratio of PGE-2 and PGI-2.

Image 2: Bayer probably won't like it if everyone would start eating grass-fed beef. After all, that would probably reduce the sales of their COX-inhibitor Aspirin protect.

For those of you wondering about a) what those prostaglandins are and / or b) why you would want to modulate their ratio and not eradicate them completely, here is is brief rundown on one of my favorite topics, the Yin&Yang of life and, on a related note, the fallacy of common black-or-white thinking. As with almost everything there are also two sides (in fact there are many more ;-) to the inflammatory coin and PGE-2 and PGI-2, two acronyms that differ by only a single letter, are situated on those opposing sides. If they are expressed at the right ratio, everything is fine. The (relative) over-expression of PGE-2 that is commonly observed in people following the "Western diet", on the other hand, is associated with a host of pathologies, such as elevated risk for color ectal cancer, suppression of ovulation, and increased problems with rheumatoid arthritis and headaches. (Relative) underexperssion of PGI-2, the other hallmark result of the "food" people are poisoning themselves with on a daily basis, in turn, increases the risk of thrombosis and stroke. If any of that does ring a bell, but you do not know which one, you may want to check out the label of your Aspirin tablets - as a cyclooxygenase inhibitor Aspirin also blocks the production of PGE-2... but before you do now pop another of those tabs, I suggest you read on and learn that by paying a few extra bucks for "real meat", you will probably never have to take your daily dose of Aspirin protect.

And while the scientists were right, grass-fed bison is in fact better than grain-fed beef, a closer analysis of their results will show that the often-heard and widely believed statement that "bison is the best form of red meat you can possibly find" is nothing but another of the 1001 dietary fairy-tales of the bloggosphere.

Figure 1: Fatty acid content of the diet (in g per 100g of the whole chow) - saturated, mono- and polyunsaturated fatty acids (n3, n6), left; CLA content, right (data adapted from Broughton. 2011)

But let's first take a look at the experimental diets, the male CD-1 mice were fed for 14 days. What is interesting about these, is that, due to the inclusion of standard rodent chow, the differences in fatty acid composition between the grass-fed vs. corn-fed bison and beef diets and the diets that were based on (wild-type) elk and commercial chicken breast meat were actually not very pronounced (cf. figure 1). And while the inclusion of corn oil in every diet may sound blasphemic in the ears of the hard-core anti-grain croud (I know you are out there ;-), the addition of grass-fed meat to an otherwise standardized (and probably suboptimal) diet is actually a strength of the study. Thusly, the study does reflect pretty well, what could happen, if the average Joe or Jane did nothing else, but replace the corn-fed meat in his/her diet with meat from range-fed animals - and wouldn't you agree that this is a much more realistic scenario than living on nothing but grass-fed beef or bison?

Figure 2: Modulatory effect of 2 weeks on prostaglandin expression of mice after two weeks on diets enriched with range-fed, or feedlot fed meat of different sources (data adapted from adapted from Broughton. 2011)

And, if we focus solely on the PGE-2 to PGI-2 ratio (you can read up on its importance in the red box above), it is obvious that a small dietary change from grain- to grass-fed meets could actually have pretty profound effects on your (auto-)immune health. The data also shows that the "healthy" lean chicken breast your nutritionist has probably told you to eat actually should not be your first choice, when it comes to establishing a healthier prostaglandin milieu - and if you don't believe me, maybe you want to trust Broughton et al.'s judgement:

[...] chicken is promoted for its health benefits, yet in our study, it was no better for possible prevention of PGE 2-associated immune pathophysiology. Furthermore, chicken would not be as beneficial as grain-fed beef and elk consumption in reducing thrombos is and stroke potential.

So, while eating (commercially raised) chicken won't harm you, it will not help you steer your inflammatory response into either the PGE or the PGI direction. Broughton, Rule and Handrich are thusly right, when they conclude that

Based on results of the present study, consumption of any of the range-fed meat sources examined would be better at reducing the possibility of immune-related pathophysiologies than meat from grain-fed cattle. [...] Although range-fed beef and bison consumption would be equivalent for their immune-based role, consumption of range-fed beef would be better for the prevention of thrombosis and stroke.

Now, isn't that surprising? Chicken not the best thing you can eat? The "healthy alternative to beef" that has been pimped in the mass media lately only on par with plain beef and superior as far as reduction in the risk of stroke and thrombosis are concerned?

Could it really be possible that the "bad red meat" is not so bad, after all? Is there the remote possibility that it's not red meat per se, but sick meat, or I should say the meat of animals we have been making sick by feeding them the same "healthy whole grains" with which we have been poisoning... ah, I mean nurturing *rofl* ourselves over all these years that is giving us migraines, arthritic joints, cancer, strokes and a whole host of nasty autoimmune diseases? I guess, I will leave it up to you to find and answer to that question ... and I am confident that you are smart to one and one, or rather grain-fed meat and (auto-)immune disease together ;-)

N3-PUFA Beneficial Only When Combined With Antioxidants

All of you who have been following this blog, lately, will have noticed that I tend to be skeptic whether fish oil and other PUFA supplements are recommendable without certain reservations. A recent study by Filaire et al. (Filaire. 2011) seems to support the view that poly-unsaturated fatty acids increase the potential for oxidative damage and should thus be combined with appropriate amounts of antioxidants to "compensate" this effect.

Over a period of 6 weeks the researchers supplemented a group of 36 judoists with either 600 mg EPA and 400 mg DHA per day or the same amount of long chain polyunsaturated fatty [LCPUFA] acids plus 30 mg vitamin E, 60 mg vitamin C and 6 mg β-carotene and measured resting and exercise-induced lipid peroxidation in their subjects. Here are the results:

At T (1) [before supplementation], there were no significant differences among treatment groups with respect to lipid peroxidation, lag phase, and levels of α-tocopherol or retinol. The consumption of an n-3 LC PUFA supplement increased oxidative stress at rest and did not attenuate the exercise-induced oxidative stress. The addition of antioxidants did not prevent the formation of oxidation products at rest. On the contrary, it seems that the combination of antioxidants added to the n-3 LCPUFA supplement led to a decrease in, CD(max) [conjugated dienes], R (max) [maximum rate of oxidation], and POOL [lipoperoxide ] and MDA [malondialdehyde] concentrations after a judo training session.

So, in a way LCPUFA work like "exercise in a pill": At rest, they increase similar stressors as exercise does. This holds true regardless of additional anti-oxidant supplementation. When you exercise, however, a combination of LCPUFA + antioxidants appears to provide some protection from exercise induced stressors, so that overall, athletes would probably benefit from LCPUFA + antioxidants consumption.

Notice, I purposefully wrote "consumption" and not "supplementation", because let's be honest: If we have a look at the combination of nutrients a natural diet would provide, you always get your LCPUFAs with adequate amounts of antioxidants. So, keeping or switching to a healthy diet should still be your priority - if you then still see the need for additional supplementation, you may want to give a quality fish oil and some vitamins a try.

Don't Blame Your Parents for Getting Fat: N-3 Fatty Acids May Save You!

Figure 1: Chemical Structure of
Alpha-Linolic Acid (HMDB v2.5)

It has been assumed that bad dietary habits of mothers-to-be increase the risk of their offspring to become obese. As Oosting et al. (Oosting. 2010) report the consumption of a diet high in n-3 Long-chain polyunsaturated fatty acids (n-3 LCP) may well prevent you from this fate, even if your mother was a fast food maniac:

A n-3 LCP-rich diet during postnatal life not only reduced fat accumulation by approximately 30% during the WSD [western diet = high fat, high carb] challenge from PN42 to 98 (p<0.001), but also led to a healthier plasma lipid profile, healthier plasma glucose homeostasis and less hypertrophic adipocytes compared to CTRL. This study shows that postnatal nutrition has programming effects on adult body composition and metabolic homeostasis. Additionally, it emphasizes that moderate alterations in fat quality during early postnatal life considerably affect adult metabolic health.

Well, to be honest these results won't really help you if already are fat, but if its still bearable they might well help you to preserve the status-quo.