Dukan Diet

Greetings all. My Spirits and Energy levels are good.

I have a lot on my plate at work.......... and not for lunch lol!!! Yes, I am rocking and rolling. I have other endeavors going on that I dont know if I want to share at this time. I have been very public, so I dont know how far I will go. I only really know a hand full of yall and thats OK. Some of you I have met in person, some I have talked to over the phone, some by email and most by the comment section on my blogs. Well thats OK. I dont force anyone to reveal who they are publicly, but I cant help wondering who you really are. I have grown to really enjoy some of the folks who regularly post comments here and my other blog. All those who came over and joined here from the Zero Carb blog. I really did not know what kind of reception I was going to get with the new blog. Let me tell you it has been a true pleasure to see the results so far.



Anyway I wish everyone well and drop me an email if you wish, no pressure, no worries. Kick your shoes off, sit back, relax and enjoy the show. HA!

Here we go:


Results thus far:

(Please let me know if I mess up on my math below, I might add or subtract incorrectly)

Day 01 = (0.0) = 00.0 lbs loss current weight: 190.0 lbs (just starting)
Day 02 = (2.0) = 02.0 lbs loss current weight: 188.0 lbs (nice)
Day 03 = (1.6) = 03.6 lbs loss current weight: 186.4 lbs (this is how we do it)
Day 04 = (1.8) = 05.4 lbs loss current weight: 184.6 lbs (lovely)
Day 05 = (1.2) = 06.6 lbs loss current weight: 183.4 lbs (interesting)
Day 06 = (1.8) = 08.4 lbs loss current weight: 181.6 lbs (oh, yeah)
Day 07 = (1.2) = 09.6 lbs loss current weight: 180.4 lbs (keep it coming)
Day 08 = (0.4) =  10.0 lbs loss current weight: 180.0 lbs (Battle On!!!)
Day 09 = (0.8) =  10.8 lbs loss current weight: 179.2 lbs (Yo!)
Day 10 = (0.8) =  11.6 lbs loss current weight: 178.4 lbs (OK?)
Day 11 = (1.0) =  12.6 lbs loss current weight: 177.4 lbs (OK part 2)
Day 12 = (1.2) =  13.8 lbs loss current weight: 176.2 lbs (OK part 3)
Day 13 = (0.8) =  14.6 lbs loss current weight: 175.4 lbs (Jeez)
Day 14 =(+4.0) = 10.6 lbs loss current weight: 179.4 lbs (Just Shoot Me)
Day 15 =(+0.4) = 10.2 lbs loss current weight: 179.8 lbs (Hold the Line!!!)
Day 16 =  (1.0) = 11.2 lbs loss current weight: 178.8 lbs (Fighting Back)
Day 17 = (1.4) =  12.6 lbs loss current weight: 177.4 lbs (brig it on!)
Day 18 = (1.2) =  13.8 lbs loss current weight: 176.2 lbs (this is how we do it)
Day 19 = (1.0) = 14.8 lbs loss current weight: 175.2 lbs (talk to me)
Day 20 = (0.8) = 15.6 lbs loss current weight: 174.4 lbs (Oh my, my)
Day 21 = (1.0) = 16.6 lbs loss current weight: 173.4 lbs (all time LOW!)
Day 22 = (0.8) = 17.4 lbs loss current weight: 172.6 lbs (how low can you go?)
Day 23 = (1.0) = 18.4 lbs loss current weight: 171.6 lbs (My eyes have seen the glory)

So I am hanging in there or am I? HA! I am sure enough am. This is an extremely busy time for me.

Have a Healthy Day my Friends and Family. Challenges come, Challenges go, but life is everlasting. Keep the Faith and Battle On!!!

Todays Menu: Black coffee, H20, Seltzer Water, Bulletproof Coffee and Smoked Chicken.

Never say DIE




Cheers,

Dave

Asian foods are low in SFAs. So the researchers had to add it to the pan.

From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
Dont worry, todays article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)

In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Talking about "test meals" (I dont like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:

• in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1; 
• in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3

Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.

Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)

Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).

"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)

The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
References:

• Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
• Edholm, T., et al. "Differential incretin effects of GIP and GLP‐1 on gastric emptying, appetite, and insulin‐glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
• Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
• Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
• Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.

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).