Dukan Diet

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 whats 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 didnt do: They supplied their rodents with diets with different fatty acid profiles.
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 - thats 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)

Whats more, its 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?
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).

You as a SuppVersity reader should know that there is no "instant gratification" with  "doing cardio" and that doing it "in the zone" is totally 90s... 1990s, even ;-)

For decades, the "Fat Burning Zone" has been one of the holy grails of exercise sciences. Then somebody realized that maximizing the ratio of fat : glucose thats are being used as fuel during a workout doesnt really have an effect on weight loss and all of a sudden papers with titles like "Changes in peak fat oxidation in response to different doses of endurance training" (Rosenkilde. 2013) have become a rarity... although, if you look closely, you will realize that this is actually not another investigation into the realms of the "Fat Burning Zone", but an afford to quantify the effect of regular "cardio training" on your bodies ability to oxidize fat, instead of glucose.

Dont worry its not really about the "fat burning zone"

Luckily Rosenkildes most recent paper, which happens to be the third spinoff of the high (600kcal/day) vs. medium (300kcal/day energy expenditure from "cardio") training volume that already taught us (you can read more about the exact exercise protocol in the previous SuppVersity articles, below) ...

• Learn more about the "Fallacy of Working Out To Burn Calories"

  how futile it is to work out like a maniac if fat loss is your goal ("Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!" | read more) and 
• how messed up the die hard belief that "exercise" just makes you hungry actually is and what the effects of endurance exercise on appetite and energy intake are ("Exercise: Does It Really Make You Hungry? The More You Train, The Less Hungry You Are." | read more)

In this second serving of the data, we can now learn whether regular endurance training increases peak fat oxidation in a dose-dependent fashion.

Figure 1: Pre & post respiratory exchange ratio (lower value = higher ratio of fatty acid : glucose oxidation) in sedentary control and 300kcal/day group, left; changes in the expression of mitochondrial enzymes (Rosenkilde. 2013)

As you can see in Figure 1 the outcomes of the experiment were not exactly surprising: While there was a persistent increase in fatty acid oxidation and the expression of the facilitative mitochondrial complexes, i.e. enzymes in the mitochondrial respiratory chain, the daily endurance training volume (MOD: 300kcal/day vs. HIGH: 600kcal/day energy expenditure during endurance training) had no effect on the effect size.

So, if its not the volume, what determines the increase in fatty acid oxidation?

Rosenkilde have probably asked themselves something similar to the above, when they realized that there were no meaningful differences between the subjects in the medium vs. high dose cardio groups. The statistical analyses the researcher conducted did yet reveal, that

• VO2peak, generally regarded as a marker of cardio-respiratory fitness,
• fat free mass, the weight of everything (incl. bones, organs, etc.) thats not fat, 
• cycling efficiency, the power output at a given VO2 peak, and the
• mitochondrial complexes II–V, enzymes that facilitate the oxidation of fatty acids,

were all associated with higher increases in fatty acid oxidation, while the observed changes in fasting plasma insulin, glucose, FFA, or glycerol had no prognostic value with respect to the increase in fatty acid oxidation.
References: 

• Crane, J. D., MacNeil, L. G., & Tarnopolsky, M. A. (2013). Long-term Aerobic Exercise Is Associated With Greater Muscle Strength Throughout the Life Span. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 68(6), 631-638.
• Harber, M. P., Konopka, A. R., Douglass, M. D., Minchev, K., Kaminsky, L. A., Trappe, T. A., & Trappe, S. (2009). Aerobic exercise training improves whole muscle and single myofiber size and function in older women. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 297(5), R1452-R1459.
• Ozaki, H., Loenneke, J. P., Thiebaud, R. S., Stager, J. M., & Abe, T. (2013). Possibility of leg muscle hypertrophy by ambulation in older adults: a brief review. Clinical interventions in aging, 8, 369.
• Rosenkilde, M., Reichkendler, M. H., Auerbach, P., Bonne, T. C., Sjödin, A., Ploug, T., & Stallknecht, B. M. (2014). Changes in peak fat oxidation in response to different doses of endurance training. Scandinavian Journal of Medicine & Science in Sports.