Sigh. Okay, here we go. It's the weekend and I'll correct the typos when I get chance!
Better read
Dr Davis' post here here to get the lie of the ground before reading this post. Now, before we get to the
Spanish study, let's look at the insulogenic effect of cream (the closest I can find to butter in a study which, unlike the Spanish study, controlled its variables). Please bear in mind that cream contains small amounts of both casein and lactose. So does butter. BTW look what casein does to insulin. But it doesn't budge glucose levels (they should drop!) so there has to be a counter regulatory system here, glucagon was not measured. It's not relevant to the role of palmitic acid in the Spanish study, but it's interesting never the less.
Taken from Dandona's paper
here. This is the effect of 300kcal of cream (equivalent to about 30g of butter) or the equivalent in casein calories:
Okay, on 300kcal of cream alone insulin "spikes" from 39.6pmol/l to 49.2pmol/l at 1h (remember the casein and lactose?) and then insulin drops below baseline at 2h and 3h.
During this period there will be palmitic acid in to the blood stream and muscles. Palmitic acid is the primary metabolic signal to switch from glucose burning to fat burning. Because essentially zero carbohydrate is supplied with cream there is neither a rise in blood glucose or in insulin.
The Spanish study uses about 40g of carbohydrate (22% of about 800kcal) with their fat load. It gets eaten along side just under 60 grams of fat or oil.
The rise in glucose is trivial for all groups. It is neither statistically nor biologically significant. We can ignore it.
Now, let's look at insulin. The full figure and caption is
here
Butter is the black squares.
Obviously, the best meal for minimising insulin response is the control meal. That's the one with round dots. That's the one we should eat to maximise weight loss, if it is a simple matter of minimising insulin! Ah, but the control meal is 40g of carbohydrate and no fat at all! Eating just 40g of carbs before an eight hour fast drops your insulin levels all right, this is starvation! But does it allow weight loss? Calories in, calories out, 40g of carbohydrate is only roughly 170kcal.
To answer this we have to look at the free fatty Acids (FFAs):
The study started with FFAs around 500micromol/l in all groups. The carb-only 40g snack DROPPED FFAs from fasting levels of 500micomol/l down to 150micomol/l at 2hours and it took until 5 hours for FFAs to get back up even close to the fasting levels seen at the start of the experiment. After a 40g fat-free carbohydrate "snack" the only source of FFAs is lipolysis and we can say that the small 40g carb snack blunts lipolysis, and so weight loss (rather I should say fat loss), for 5 hours! And you're hungry too.
Now the butter group produced the least fall in FFAs while the insulin was elevated from the carbohydrate and also allowed the most sustained rise in levels of FFAs once the carbs were dealt with. The FFAs were still significantly elevated at the end of the study. The area under the curve for chylomicrons (no VLDLS involved in this study) is also bigger and peak chylomicron-triglyceride level is higher in the butter group than after any other fat meal.
Butter provides palmitic acid which is the physiological signal to switch from using glucose to using fat. It also provides medium chain triglycerides which will produce ketone bodies for a few hours, which also produce physiological insulin resistance and a rise in insulin in their own right.
So in the presence of 40 grams of carbohydrate extra insulin is need to maintain normoglycaemia. The insulin should inhibit lipolysis. It certainly does in the 40g carbohydrate snack group! What about the butter group? The butter provides plenty of FFAs to run metabolism on and storing some calories is no big deal. But does this insulin effectively store calories? What if the adipocytes become physiologically insulin resistant with palmitc acid in exactly the same way as muscle cells do?
You know, my mantra: The function of insulin is the inhibition of lipolysis.
This study makes it look as if it is not quite that simple.
In fact, you have to ask some interesting questions about exactly where all of these FFAs come from and where the chylomicrons go to. ALL of the fat meals provided the SAME number of fat calories, but the FFA levels in the butter group where ALWAYS higher than other fat meal groups, even before chylomicrons levels became different between groups. Now, FFAs do not pop in to existence merely to prove that butter is going to kills us through obesity. They come from SOMEWHERE. And chylomicrons. These are lower in the oil meal groups than in the butter meal group. Where are the chylomicrons going to? Because all fat based meals provide the same number of fat calories then either:
a) the butter group has to be allowing more lipolysis from adipocytes or from chylomicrons to get those extra FFAs. Lipolysis means fat loss.
or
b) the non-butter groups are allowing more fatty acid storage and less FFA release. Insulin sensitive fat cells store fat! Low FFAs means less fat release. You CANNOT burn fat without lipolysis!
As I see it butter produces sustained chylomicronaemia. The chylomicrons are used to provide FFAs to run metabolism on rather than going in to storage. There is no hyperglycaemia to glycate apoB48s, so who cares if they hang around. Either they (or possibly adipocytes) are supplying energy.
Oil based meals can only produce lower levels of chylomicrons if they are storing the chylomicron fat ON YOUR BUTT and lowered FFAs means the INHIBITION of lipolysis from chylomicrons or from YOUR BUTT.
There is no other explanation that I can see, whatever the insulin levels are. Take you pick.
More fat gain and/or less fat loss: The gift of olive oil!
To summarise:
Insulin controls bodyweight. Physiological insulin resistance modifies this.
Of course if you think apoB48 was evolved to kill you, run from the butter and knock back the vegetable oil/fish oil combination. Maybe cut a few calories too!
Me, I'll stick to FFAs and butter as my energy source.
Peter
BTW 40g is close to the total daily carb intake for a reasonable LC diet. After that it's fat on its own and, as we all well know, fat on it's own causes ZERO insulin spike and allows FFA run metabolism where fat can be both stored and accessed freely. Okay, add a little protein somewhere along the line.
Okay, on 300kcal of cream alone insulin "spikes" from 39.6pmol/l to 49.2pmol/l at 1h (remember the casein and lactose?) and then insulin drops below baseline at 2h and 3h.
During this period there will be palmitic acid in to the blood stream and muscles. Palmitic acid is the primary metabolic signal to switch from glucose burning to fat burning. Because essentially zero carbohydrate is supplied with cream there is neither a rise in blood glucose or in insulin.
The Spanish study uses about 40g of carbohydrate (22% of about 800kcal) with their fat load. It gets eaten along side just under 60 grams of fat or oil.
The rise in glucose is trivial for all groups. It is neither statistically nor biologically significant. We can ignore it.
Now, let's look at insulin. The full figure and caption is here
Butter is the black squares.
Obviously, the best meal for minimising insulin response is the control meal. That's the one with round dots. That's the one we should eat to maximise weight loss, if it is a simple matter of minimising insulin! Ah, but the control meal is 40g of carbohydrate and no fat at all! Eating just 40g of carbs before an eight hour fast drops your insulin levels all right, this is starvation! But does it allow weight loss? Calories in, calories out, 40g of carbohydrate is only roughly 170kcal.
To answer this we have to look at the free fatty Acids (FFAs):
The study started with FFAs around 500micromol/l in all groups. The carb-only 40g snack DROPPED FFAs from fasting levels of 500micomol/l down to 150micomol/l at 2hours and it took until 5 hours for FFAs to get back up even close to the fasting levels seen at the start of the experiment. After a 40g fat-free carbohydrate "snack" the only source of FFAs is lipolysis and we can say that the small 40g carb snack blunts lipolysis, and so weight loss (rather I should say fat loss), for 5 hours! And you're hungry too.
Now the butter group produced the least fall in FFAs while the insulin was elevated from the carbohydrate and also allowed the most sustained rise in levels of FFAs once the carbs were dealt with. The FFAs were still significantly elevated at the end of the study. The area under the curve for chylomicrons (no VLDLS involved in this study) is also bigger and peak chylomicron-triglyceride level is higher in the butter group than after any other fat meal.
Butter provides palmitic acid which is the physiological signal to switch from using glucose to using fat. It also provides medium chain triglycerides which will produce ketone bodies for a few hours, which also produce physiological insulin resistance and a rise in insulin in their own right.
So in the presence of 40 grams of carbohydrate extra insulin is need to maintain normoglycaemia. The insulin should inhibit lipolysis. It certainly does in the 40g carbohydrate snack group! What about the butter group? The butter provides plenty of FFAs to run metabolism on and storing some calories is no big deal. But does this insulin effectively store calories? What if the adipocytes become physiologically insulin resistant with palmitc acid in exactly the same way as muscle cells do?
You know, my mantra: The function of insulin is the inhibition of lipolysis.
This study makes it look as if it is not quite that simple.
In fact, you have to ask some interesting questions about exactly where all of these FFAs come from and where the chylomicrons go to. ALL of the fat meals provided the SAME number of fat calories, but the FFA levels in the butter group where ALWAYS higher than other fat meal groups, even before chylomicrons levels became different between groups. Now, FFAs do not pop in to existence merely to prove that butter is going to kills us through obesity. They come from SOMEWHERE. And chylomicrons. These are lower in the oil meal groups than in the butter meal group. Where are the chylomicrons going to? Because all fat based meals provide the same number of fat calories then either:
a) the butter group has to be allowing more lipolysis from adipocytes or from chylomicrons to get those extra FFAs. Lipolysis means fat loss.
or
b) the non-butter groups are allowing more fatty acid storage and less FFA release. Insulin sensitive fat cells store fat! Low FFAs means less fat release. You CANNOT burn fat without lipolysis!
As I see it butter produces sustained chylomicronaemia. The chylomicrons are used to provide FFAs to run metabolism on rather than going in to storage. There is no hyperglycaemia to glycate apoB48s, so who cares if they hang around. Either they (or possibly adipocytes) are supplying energy.
Oil based meals can only produce lower levels of chylomicrons if they are storing the chylomicron fat ON YOUR BUTT and lowered FFAs means the INHIBITION of lipolysis from chylomicrons or from YOUR BUTT.
There is no other explanation that I can see, whatever the insulin levels are. Take you pick.
More fat gain and/or less fat loss: The gift of olive oil!
To summarise:
Insulin controls bodyweight. Physiological insulin resistance modifies this.
Of course if you think apoB48 was evolved to kill you, run from the butter and knock back the vegetable oil/fish oil combination. Maybe cut a few calories too!
Me, I'll stick to FFAs and butter as my energy source.
Peter
BTW 40g is close to the total daily carb intake for a reasonable LC diet. After that it's fat on its own and, as we all well know, fat on it's own causes ZERO insulin spike and allows FFA run metabolism where fat can be both stored and accessed freely. Okay, add a little protein somewhere along the line.
