Dukan Diet

Day 308.

Ive made two chili recipes already this year, but when I read Kalyns post listing the ingredients for the Obama family chili, I was intrigued. Cumin? Turmeric? In chili?

This I had to make.

The result is a mild and pleasant chili, suitable for all ages. The kids gladly ate this, and not once complained about spice---a complaint that is quite common at our dinner table. Adam and I added a few drops of Tabasco sauce to our bowls.

We are having friends from Australia over tomorrow, and I look forward to a feast with this chili and McCains ribs.

The Ingredients.

--1 can kidney beans (and the goop!)
--1 lb lean ground meat (I used ground chicken)
--1 green bell pepper, chopped
--1 large onion, chopped
--5-6 medium tomatoes, chopped (include seeds and all)
--4 chopped cloves of garlic
--1 tsp cumin
--1 tsp oregano
--1 tsp basil
--1 tsp turmeric
--2 tsp chili powder (I started with 1, but added another after a few hours. Do whats right for your family)
--1 tsp salt
--3 T red wine vinegar


The Directions.

I used a 6 quart Smart Pot for Obamas chili.

I made the executive decision to increase all of the spices from the original recipe, because in CrockPot cooking, the slow simmer of the ingredients cooking can overpower added spices. Im glad that I upped everything---the flavors were there, but they were subtle and not overpowering.

I gave myself a pat on the back.

I also decided to not brown the meat on the stove top. I hate browning meat, and since the chicken I used was quite lean, I just crumbled it in raw. If you are going to use beef, or enjoy browning meat, go for it.

Chop up the tomatoes, garlic, onion, and bell pepper. Add to the crockpot. Open the can of beans, and pour in the whole thing. Add the ground meat. Stir in all of the spices and the red wine vinegar.

Cover and cook on low for 7-9 hours, or on high for 4-5. I cooked our chili on low for 9 hours.

Season with a bit more salt, to taste.

Obama serves his chili over rice, so we did too. The kids really liked that a lot----they love white rice.

The Verdict.

Very tasty! It does not pack a punch the way traditional chili does, which was a pleasant change. I loved the addition of cumin and turmeric---I am new to turmeric, and like how it turns things orange.

Were going to have the leftovers as taco filling.

Remember to vote!

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
psst. just like yesterday, I will not post any comments with a political slant. ;-o

Day 249.

Chicken pot pies are a staple in a lot of homes---it started as a way to use up all the leftovers from the fridge, but now has changed into a meal made all on its own.

I havent had very many pot pies. Ive never ordered one at a restaurant, and am only really familiar with the frozen ones put out by Marie Callenders. I figured that since the tamale pie and the bbq chicken topped with cornbread transferred so nicely to crockpot cooking, a chicken pot pie would too.

Adam thought it tasted like stuffing. It kind of did. My taste buds are all out-of-whack from a funky cold. Everything kind of tastes like metal.

The Ingredients.

Filling:
--2 chopped up skinless chicken thighs or breast halves (raw, but chopped up)
--1/2 cup chopped carrots (these were fresh, but frozen would work)
--1/2 cup frozen corn
--1/2 cup frozen peas
--1/2 t marjoram
--1/2 t thyme
--1/2 t celery seed
--1 t onion powder
--canned cream-of-something soup (or see homemade alternative down below)
--2 T low fat milk

Homemade Soup Alternative:
make a roux on the stove top with the butter and flour, then whisk in the other ingredients.

--1 T butter
--3 T flour (Pamelas or other GF baking flour)
--1/2 cup low fat milk (I used soy)
--1/2 cup chicken broth
--1/4 t salt
--1/4 t black pepper

Biscuit Topping:

--2 cups biscuit mix (I used Bobs Red Mill biscuit mix. I much prefer Pamelas but my favorite store has been out of it for a few weeks)
--1/2 T white sugar
--1/2 cup melted butter (thats a whole stick)
--3/4 cup low fat milk (stick with 2% or lower; I used soy)

The Directions.

Im already tired of typing. This is a long one. Sorry.

I used a 4 quart crockpot for this recipe. There really wasnt too awful much filling---I used what I had on hand, but if you have a large family or would like leftovers, Id double the filling.

Spray crockpot with cooking spray. Chop up the chicken and put it into the crockpot. Dump in the vegetables. Add all of the spices. Stir in the cream-of-something soup and add 2T of milk to the can, squish it around to get all the good stuff out of the can, and pour in the rest. Stir well.

In a mixing bowl, make up the biscuit topping. The dough will be pretty playdoughy, and I pretty much mixed it with my hands. Spread the dough on top of the chicken and veggie mixture.

Cover and cook on high for 3-5 hours, or on low for 6-7. This is done when the biscuit topping is golden brown, and is hard to the touch in the middle. I cooked ours on high for 4 1/2 hours, and it got a bit too crunchy on the very edges.

If you find that your crockpot seals really well and you have a bunch of condensation building up, you can prop open the lid with a wooden spoon or chopstick. I tried the paper towel trick with this dish, and wasnt impressed. I laid a double-layer of paper towels over the top of the crock, then put the lid back on. The condensation made the paper towels really wet, and they drooped into the food. Also, when I took off the lid and then removed the towels (they were very wet and very hot) I got a blast of steam on my hand that hurt. Im going to stick with venting with a chopstick.

The Verdict.

This was neat to try, and Im glad that I did, but I dont see making it again unless someone specifically requests it. Were just not huge chicken pot pie people. My brother really likes chicken pot pie though. I should make it for him. I love it that with stuff like this you can play around and use whatever meat and veggies you have in the house.

The filling was good. Adams right, it tastes like stuffing. Is that the marjoram?

This plan was developed by  NASA to help astronauts lose weight quickly before a mission in space. What is the Cosmonaut regime? Who is he? We take you into space, follow us!
Cosmonaut regime, what is it?
Originally developed by an American doctor for space adventurers, it quickly became a diet program praised by many women in search of a perfect figure.

Cosmonaut diet is a low calorie diet that is low in calories, very strict and very difficult to follow.


The basic rules of the Cosmonaut regime
The first idea to lose weight is to drink water.
Plenty of water. Or tea infusion or coffee. At least 2 liters a day.

It also removes the power of fatty materials such as oil, margarine, butter.

Shelved in favor of sugar sweeteners!
We can dress salads with lemon, mustard or vinegar.

And complete the Cosmonaut regime vitamin supplements and minerals.




Example of the menu system Cosmonaut
Breakfast:
Coffee or tea.

lunch:
3 hard boiled eggs and a tomato or 1 fillet grilled meat (200 g) and a green salad.

dinner:
1 grilled fillet (200g) and a green salad or ham fat York (150 g) and 1 skimmed yogurt.


Cosmonaut system: effectiveness and limitations
This scheme is ultra restrictive.
One can hardly eat anything during the diet.
Suffice to say that it is very difficult to follow ...
Fatigue failures and yo-yo will certainly be felt.
Even if weight loss can be spectacular (almost 3 pounds in 3 days only), watch the boomerang effect!

Borrelia burgdorferi Sticks to Host Cells via Heparin-binding Proteins

A research group at the University of Calgary has watched the binding of fluorescent Borrelia burgdorferi spirochetes, the Lyme disease pathogen, to the surface of blood vessels in mice. (ref. below) A small heparin molecule was shown to block this interaction between the spirochete surface protein BBK32 and the heparan sulfate proteoglycans of the endothelial cells of the skin blood vessels.

The heparin-binding domains in the spirochete protein, BBK32 are easy to spot in the amino acid sequence of this protein that I downloaded from the NCBI protein database:

>gi|19072701|gb|AAL84596.1| BBK32 [Borrelia burgdorferi]
MKKVKSKYLALGLLFGFISCDLFIRYEMKEESPGLFDKGNSILET
SEESIKKPMNKKGKKIARKKGKSKVSRKEPYIHSLKRDSANKSN
FLQKNVILEEESLKTELLKEQSETRKEKIQKQQDEYKGMTQGSL
NSLSGESGELKETIESNEIDITIDSDLRPKSSLQDIAGSNSISYTDE
IEEEDYARYYLDEDDEDDEYYEDDYEEIRLSNRYQSYLEGVKYNV
DSAINTINKIYDTYTLFSTKLTQMYSTRLDNLAKAKAKEEAAKFTK
EDLEKNFKTLLNYIQVSVKTAANFVYINDTHAKRKLENIEAEIKTL
IAKIKEQSNLYEAYKAIVTSILLMRDSLKEVQGIIDKNGVWY
Basic amino acids are K=lysine, R=arginine

The minimal heparin binding pairs, e.g. KKVKSK are shown in red and the strong heparin-binding triplets, e.g. KRK, are shown in blue. Notice that one triplet is augmented with several pairs to further enhance heparin binding.

I would also expect that BBK32 would be internalized into host cells and transported into the nucleus, where it may alter transcription, a la HIV-TAT. The existence of multiple, strong heparin-binding domains may also serve to bind the BBK32 (or the spirochetes) to multiple different heparan sulfate proteoglycans and interfere with the HSPG circulation system. This may have a toxic effect.

reference:
Norman MU, Moriarty TJ, Dresser AR, Millen B, Kubes P, Chaconas G. Molecular mechanisms involved in vascular interactions of the Lyme disease pathogen in a living host. PLoS Pathog. 2008 Oct 3;4(10):e1000169.

One of my favorite options for a quick healthy lunch is this Spicy Avocado in Pita.

Click to continue reading

It takes pains to maintain your gains!

You will certainly remember the shocking revelation that simply eating more protein is not going to prevent the diet induced muscle loss that occurs whenever you consume less energy than you expend (read up on "Protein Intake & Muscle Catabolism: Fasting Gnaws on Your Muscle Tissue and Abundance Causes Wastefulness" | go for it!)...

Dont rejoice, the study at hand does not refute this - protein is still unable to counter the increase in atrogin-1 and other muscle cannibalizing proteins, but there is a "tweak" by the means of which you can at least avoid that its pro-anabolic affects are also impaired.
What this "tweak" is? Well, thats easy: Heavy lifting. If you are familiar with the "muscle loss in zero gravity" research that has been conducted by and for the NASA in the past decades (e.g. Ferrando. 2002).this shouldnt surprise you. The NASA studies have after all shown quite conclusively that compared to bed-rest / chronic skeletal muscle unloading, starving yourself is almost "anabolic". No wonder that lifting heavy objects, and not dietary protein is the #1 when it comes to saving your muscular ass from shriveling away on a long and hard diet.

Why does resistance training work, if protein fails?

As discussed in "Protein Intake & Muscle Catabolism" (read it!), its not a question of the pro-anabolic effects. You, as a suppversity reader know that the p-AKT/mTOR pathway thats activated by protein feeding is sufficient to increase the influx of protein into the musculature. What your beloved protein cant do, though, is to reset a different switch: The "sacrifice muscle to fuel more fundamental metabolic demands switch" which is triggered whenever you are in a long(er) term energy deficit.

"Training For Gains: High Intensity, Low Volume Strength Gains Stick." | more

So what can be done then? Well,... as it is so often the case, the answer lies - once more - open before our eyes: Hit the weights, down the protein and kick your diets catabolic ass!

I know this sounds too easy, but if you take a peek at the weight loss diets of the average physique athlete and their appearance on stage, it stands out of question that the combination of resistance training and strategic protein supplementation spares muscle mass.

Now the verb "to spare", according to the Oxford English Dictionary, means "to leave (a person) unhurt" (OED.COM), which is - and you probably expected this already, not really accurate. Even the latest data from the School of Medical Sciences at the RMIT University in Melbourne and the Exercise Metabolism Research Group at the Department of Kinesiology of the McMaster University in Hamilton, Ontario, Canada, and the Canadian Sport Institute clearly demonstrates that you cannot switch the diet-induced protein wasting off, completely (Areta. 2014).

Figure 1: The large inter-individual differences make it virtually impossible to tell, whether the MURF-1 levels increased. The similarly catabolic (see overview in the middle) atrogin was yet significantly increased in the early (15g) and late phase (30g) after the workout during ED (Gumucio. 2013; Areta. 2014)

In the corresponding experiment, 16 young, healthy, resistance trained subjects (8 females, 8 males) who had been fed individualized pre-packaged meals delivering 45 kcal/kg FFM (macros: PRO / CHO / FAT 1.4-1.6, 3-3.5 and 0.5-1.5 g·kg BM) per day for five days before they went on a standardized energy 30% energy reduced diet containing approximately

• 1.4-1.6g protein per kg total body mass, 
• 4.0-4.5g carbohydrates per kg total body mass and
• 1.5-2.5g fat per kg total body mass

for another five days. At the end of this "ED" period and five days on rations with only 30kcal/kg fat free mass, all subjects performed a standardized leg press workout (warmup + 6 sets of 8 repetitions at ~80% 1 RM with 3 min rest between set) that was followed by the ingestion of either 15g or 30g of whey protein or an isocaloric placebo.

Figure 2: SLC7A5 AA transporter expression (left) and myofibrillar fractional protein synthesis (% / hour; Areta. 2014)

What a brief glance at the data in Figure 2 does tell you, though, is that resistance training will effectively counter, the diet-induced downregulation of the pro-anabolic response to protein. What it wont do, though is to increase the net protein retention to levels comparable to those on an energy balanced diet!
Contrary to what Areta et al. may have suspected the restoration of the protein synthetic response in the post-workout period did not restore the expression of the amino acid transporter gene SLC7A5 to normal. It is thus not surprising that...

Highly suggested read: " Evidence From the Metabolic Ward: 1.6-2.4g/kg Protein Turn Short Term Weight Loss Intervention into a Fat Loss Diet" | more

"[...] despite this elevation, exercise merely restored MPS [muscle protein synthesis] to a level that was similar to, but not exceeding, rates measured in EB [energy balance]. Accordingly, it appears the metabolic status of the muscle during short-term (5 days) ED [energy deficit] plus a ~10 h fast may dictate that contractile overload in isolation is not enough to increase MPS to values that otherwise would be observed when subjects are in EB." (Areta. 2014)

The results of this recent study do thus have to regarded as another nail an already boarded up coffin thats loaded with bro-scientific myths about "body recompositioning."
Unlike the non-existent changes in amino acid transporter expression, the observation that 30g of protein are more effective than 15g will probably not come as a surprise to you - notwithstanding the fac t that this was "the first [study] to determine the acute muscle anabolic response to resistance exercise with two different doses of protein ingested after exercise during short-term ED", by the way. About as unsurprising as the researchers (eventually unwarranted - I dont see a 20g protein group, here ;-) conclusion that their ...

"[...]results suggest that the optimal amount of protein to maximize the response to a single bout of resistance training while in ED may be above the level (20 g) found to maximize MPS post-exercise for individuals who are in EB." (Areta. 2014)

And my recommendation, not to worry too much about all the details. There are a couple of simple principles that have been working for generations of athletes thriving to cut weight without having to sacrifice muscle mass; and as you should know if youve read and memorized the "9 Simple Rules Every Dieter Must Follow" (go back) consuming 30g of protein with every meal and lifting heavy objects are both part of a set of rules thats rooted in bro- and supported by pro-science.
Reference: 

• Areta, José L., et al. "Reduced resting skeletal muscle protein synthesis is rescued by resistance exercise and protein ingestion following short-term energy deficit." American journal of physiology. Endocrinology and metabolism (2014). Ahead of Print.
• Ferrando, Arny A., Doug Paddon-Jones, and Robert R. Wolfe. "Alterations in protein metabolism during space flight and inactivity." Nutrition 18.10 (2002): 837-841.
• Gumucio, Jonathan P., and Christopher L. Mendias. "Atrogin-1, MuRF-1, and sarcopenia." Endocrine 43.1 (2013): 12-21.

Is there something to the good vs. bad fat shenanigan, after all?

Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter - I mean, will you get and stay lean by upping your PUFA intake? Lets take a look!
In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women - a result of which you already know that it was only partly confirmed.

Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)

The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:

• Table 1: Liquid meal nutrient composition breakdown (Clevenger. 2014).

  The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
   
• The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.
  
  
• Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 

As the data in Table 1 indicates, the nutrient profiles didnt differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that its health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand - so the ultimate question is: Does DIT even matter?
References:

• Bjermo, Helena, et al. "Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
• Clevenger, Hui C., et al. "Acute effect of dietary fatty acid composition on postprandial metabolism in women." Experimental physiology (2014): expphysiol-2013.
• Westerterp, Klaas R., et al. "Dietary fat oxidation as a function of body fat." The American journal of clinical nutrition 87.1 (2008): 132-135.

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).