Distinctive postprandial modulation of beta cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids
which was very, very carefully set up to demonstrate post prandial insulin resistance following the ingestion of the saturated fats from butter while also demonstrating a progressively improving insulin sensitivity using oils with increasing content of (mostly) linoleic acid.
A brief look at reference 15 methods section confirms they measured the test meal lipids by gas chromatography.
Obviously, to anyone lacking the Protons perspective, the clear cut message is that saturated fat causes insulin resistance. Insulin resistance is BAD. Saturated fats are BAD.
What Protons actually predicts is that resisting insulin by ingesting saturated fats limits insulin-facilitated obesity, so eliminates the subsequent adipocyte distension derived release of FFAs (which cannot be suppressed by insulin), which would lead to metabolic syndrome.
Resisting insulin prandially resists obesity and so resists obesity-derived insulin resistance. Read that very carefully.
Aside: Resisting insulin in the immediate post ingestion period is a short term effect for a few hours. It's physiological. Constant presence of FFAs secondary to increased basal lipolysis from distended adipocytes is present 24/7 irrespective of what you eat. These fatty acids supply calories and if you are eating carbohydrate then you must resist cellular glucose ingress to take in to account that FFA supply of calories. This insulin resistance is different (still the correct physiological response to FFA availability) because it follows on from pathology related to adipocyte lipid droplet size. The third type of insulin resistance is much more complicated. So is the fourth. Here is not the place to discuss them. End aside.
Sooooo. I really, really like this:
This is *not* demonstrating saturated fat induced pathological insulin resistance. Here the insulin "resistance" will simply stop you getting fat. I would define this as the "normal" response to an high fat meal, assuming a low linoleic acid based fat.
What it *is* demonstrating is pathological insulin sensitivity following the ingestion of 10.3% (actually slightly under this but close enough) of calories as linoleic acid. Here as little as 140pmol/l of insulin will rapidly clear your plasma of calories and leave you hungry. The meal is largely lost in to your adipocytes. You WILL want to eat again, and soon.
This is fundamental and simply falls out of the Protons hypothesis.
Now, there are problems with the study and the authors are to be congratulated on the result generated (though not on their conclusions of course), especially the composition and size of the meals they had to design to get there. But here we are looking at a dynamic response to a single meal. Is it possible to examine their important findings under more steady state conditions? Would the relationship of PUFA ingestion to pathological insulin sensitivity still hold?
Now, there are problems with the study and the authors are to be congratulated on the result generated (though not on their conclusions of course), especially the composition and size of the meals they had to design to get there. But here we are looking at a dynamic response to a single meal. Is it possible to examine their important findings under more steady state conditions? Would the relationship of PUFA ingestion to pathological insulin sensitivity still hold?
What would we find if we kept plasma FFAs forcibly elevated for 24h using repeated small oral fat loads supplying 2430kcal over a 24h period (but no other food) instead of a single oral ingestion of 800kcal as one mostly fat meal?
Then, instead of tracking the insulin response to a small amount of starch/protein along side the fat of the 800kcal meal, we could assess insulin sensitivity during an hyperglycaemic clamp at 20mmol/l of glucose in plasma. The more glucose needed to achieve this level, the greater the insulin sensitivity.
We are now well away from normal physiology but we are asking essentially the same question under more constrained conditions.
I'm assuming people have realised that I'm now describing Xiao's study from the last post
which produced this chart from the above protocol:
To me, the results of Xiao's study and the Spanish study concur beautifully.
Not everyone will agree with me that these reflect a core reality, I wouldn't expect that. But in my NSVHO this is how physiology works. Linoleic acid is insulin sensitising.
However, when you have confirmation bias as badly as I do, and you find two non related studies which neatly corroborate each other while confirming your biases, you know you are trapped. That's me.
You have been warned.
Peter
Addendum: Obviously palm oil at around 8% of calories as LA is already insulin sensitising, it's in the same ball park as the 10.3% LA arm of the Spanish Study. A true SFA arm to the study would need to have LA at around 2% of calories and I would predict a GIR well under 40μmol/kg/min.
