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“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
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Tuesday, October 19, 2010

Sat Fat --> PUFA = Less SubQ Belly Fat?

Mostly a bookmarking post, but I found this interesting

Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity

For some reason I can't C&P the abstract.

They analyzed the results of 5 weeks on diets rich in sat fat vs. PUFA (described as spreads and oils, presumably high in omega 6 and probably some transfats :( ) on T2's, obese and non-obese subjects.  The study size was small, but I think most readers will be as surprised as I was by the results.

All of the PUFA groups had less subcutaneous belly fat at the end of the 5 weeks. This was statistically significant in the non-diabetics, both obese and non-obese.  Visceral fat either decreased or stayed the same. This was statistically significant for the diabetics, but not the non-diabetics.  

The PUFA group seemed to eat less, but total body weight didn't change.  Not sure what that's about.  Could be underreporting or a slower metabolism?  In any case, if this can reduce belly fat .....

Insulin sensitivity IMPROVED on the PUFA diet.  

This goes counter to that n=1 "study" by the journalist that altered her diet to consume O6's that has been making the LC rounds lately.  


Mario Renato said...


Although not specific to T2Ds, but have you read:

and these Stephan posts:

Mario Renato said...

And, there is that old trial (Corn Oil in Treatment of Ischaemic Heart Disease,, the only trial that has compared sat fat, unsat fat and poly fat. Two people were excluded from the trial because of diabetes, one developed and another worsened it soon after the beginning of the study. One in the unsat fat (olive) and the other on the poly fat (corn).

CarbSane said...

Thanks for the links Mario and welcome to my blog. I've seen that first one from Stephan and will look at these others.

Right now I'm tearing my hair out trying to a study relating all LCFA to IR ... uggh ... browser crash wiped out a week of history :(:(

I do wonder if O6 is so toxic/inflammatory why the epileptics getting a corn oil diet see beneficial effects. Could be the high ketones counter the O6?

I'm not sure if you've commented before, so if I'm extending a repeat welcome sorry for that :)

Mario Renato said...


Yes, I have commented before, but a welcome is allways welcome!

There is a new trial out on this subject! It looked on sat fat and insulin sensitivity on MetS obese subjects. "Conclusion: There was no effect of reducing SFA on SI in weight-stable obese MetS subjects".

The O6 and epileptics is a hard question!

Nigel Kinbrum said...

Hi. I worry about diets that are very high in PUFAs. Have you seen Incidence of cancer in men on a diet high in polyunsaturated fat - The Lancet March 6 1971?

CarbSane said...

Hi Nige! The incidence of cancer does seem to be prevalent in the non-adherers to the experimental PUFA intervention. Not sure what to make of that! I'm by no means advocating a PUFA rich diet here. Certainly there is a lot of evidence both ways regarding these fats. I'm not sure we can separate out the effects of the PUFA's themselves from the trans-fats (partially hydrogenated oils in margarine), the chemicals involved in production of these, and fast food/commercially prepared foods that include a lot of these fats and/or involve fry baths, etc.

OTOH, the depressing part of that Lancet study: We're all going to die of something :(

CarbSane said...

Hit post too soon -- additional comment on Nige's link: There was no difference in weight change between the two groups. I think O6's as a contributing factor in the obesity epidemic is probably a "weakest link".

Nigel Kinbrum said...

Hi again. Chris Masterjohn mentions the Veterans Study in his article Precious Yet Perilous
"The researchers took care not to reuse the vegetable oil after cooking but took no such precautions with the butter, resulting in butter that was very deficient in vitamin E. There were also twice as many heavy smokers and 60 percent more moderate smokers in the butter group." Hmmm.

Ned Kock said...

One possible explanation could be O6's increasing nonexercise activity thermogenesis (NEAT), which seems to have a massive effect on body fat gain/loss:

Apparently O6's make one a bit more aggressive, and somewhat restless. There is even a theory (I need to find the reference) that increased O6 consumption evolved among humans because it increased their aggressiveness. Presumably that made them better hunters; particularly men.

If that is true, it is a major maladaptation today, because physical violence is institutionalized (e.g., police officers can use it, under certain circumstances). Without escape mechanisms like heavy physical exertion, all one is left with is a lot of stress. Obesity soon follows.

CarbSane said...

Very interesting stuff Ned. If PUFA increases aggression would it not also increase cortisol which is correlated to increased belly fat? Yet in this study the opposite was seen.

Welcome to my blog and thanks for commenting! I'll be checking out yours as well (I'm sure I've stopped by before).

CarbSane said...

@Nige: I don't think any area of obesity-related research is so full of contradictory outcomes as the whole PUFA/O6 area. I've come across lots of studies where no effect was seen, and as human nature would have it, these types of studies are largely ignored by both camps.

I've got me some belly fat. I've vastly improved the fatty acid profile of the fats I consume over the past year. It hasn't changed a thing. That's my own n=1 :)

Organism as a Whole said...

Ray Peat said that PUFAs are poison to the liver. (I think.) PUFAs increase insulin sensitivity by poisoning the liver's ability to produce free fatty acids. Decreased free fatty acids increases insulin sensitivity.

I think the cholesterol- and triglyceride-lowering effects of PUFAs are due to its toxic effects on the liver. PUFAs impair the production of cholesterol and triglycerides in the liver.

Martin Berkhan recently posted an article defending alcohol. He said that alcohol increases insulin sensitivity. I speculate it's because alcohol poisons the liver's ability to produce free fatty acids.

Another study suggested that the ratio of omega-6 to omega-3 doesn't matter. What matters is the absolute quantity of omega-3. So I don't think the benefits of omega-3 has anything to do with its anti-inflammatory properties by replacing the inflammatory omega-6 fatty acids. I think it's because omega-3 poisons the liver's ability to produce free fatty acids, thus increasing insulin sensitivity.

CarbSane said...

Hmmm OW, that is interesting. By "ability to produce free fatty acids" that would mean this "poisoning" shuts down de novo lipogenesis (DNL)? I'm curious about that theory on alcohol. I do know some T2's who drink to bring down their fasting glucose (and there's alcoholic hypoglycemia) b/c the multitasking to metabolize the alcohol reduces gluconeogenesis. But the relation of alcohol to fatty livers would seem to argue against this?

I think I've seen that study about the amount of O3 being the more important part of the equation. That has been my experience in terms of how I "feel". Actually I just found an article I'll blog on soon that lists O3's as being mildly insulin de-sensitizing.

Thanks for contributing and welcome to my blog Organism as a Whole!

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