Does a high fat diet cause insulin resistance in a diabetic ?

Over the years, certain low carb and or fat phobic low carb higher fat antis, have said a high fat diet causes insulin resistance. Many of these people who have said this, have talked about the so called pizza effect, and love to quote Gary Scheiner  a diabetic and diabetes expert. Gary has a great deal of trouble controlling his blood glucose, as detailed in my thread today called 'Nobhead aka Pinocchio never gives up' I have stated many times dietary fat does not cause insulin resistance for a diabetic and given the reasons I believe this to be true. When eating a high carb high fat diet (the worst possible combination) BG control can be difficult, because it can totally alter the insulin profile. BG can look good at one or two hours, but be way too high three, four or even more hours. The reason for this is because the fat has slowed down digestion markedly, and BG can still be rising long after the fast acting insulin has stopped doing it's job. (insulin using/injecting diabetics)

Now, knowing the low carb higher fat antis hold Gary Scheiner in such high esteem, I thought I would check out Gary's take on this, he says.

"Sometimes, food doesn't digest all that quickly. Especially when it contains a great deal of fat, or you consume a lot of it at one time. Fat slows the rate at which food empties from the stomach into the intestines, where it is then absorbed into the bloodstream. Likewise, large volumes of food take longer to pass through the stomach than smaller quantities. If you consume multiple slices of pizza, or the pizza is laden with fat-filled toppings like sausage or extra cheese, you can expect the carbs to take a few hours longer than usual to "kick in".

When we give a bolus of rapid-acting insulin (either via injection or a pump), the insulin usually starts to work in about 15 minutes, peaks in 60-90 minutes, and finishes in about three to four hours.  This activity profile works fine if the food you are eating digests fairly rapidly. When the food digests slowly, a normal meal bolus may peak too early – resulting in a blood sugar drop followed by a blood sugar rise a few hours later when the food is finally absorbed but the bolus is fading"

So, low and behold I agree very much with Gary. Now what about the insulin resistance, you may be thinking. Gary goes onto say. Link to information here. http://diatribe.org/pizza-and-blood-sugar-control-not-quite-easy-pie

"The final insult brought on by high-fat foods like pizza is the prolonged, gradual blood sugar rise that occurs many hours after eating. And guess what...it's not carbs that are causing the rise. It's the fat.  But not directly. Here's how. High fat meals and snacks cause an increase in serum triglycerides for many hours. When the liver is confronted by large amounts of triglycerides, it becomes resistant to insulin. And that results in greater secretion of glucose by the liver. Without a concurrent increase in insulin, blood sugar levels are going to go up, up, up."

This is where Gary and the Bonkers and Nobheads of this world get it wrong. A high fat low carb meal does not raise serum triglycerides, as detailed here.

"Doubling saturated fat in the diet does not drive up total levels of saturated fat in the blood, according to a controlled diet study. Increasing levels of carbohydrates in the study diet promoted a steady increase in the blood of a fatty acid linked to higher risk for diabetes and heart disease."

However, increasing levels of carbohydrates in the diet during the study promoted a steady increase in the blood of a fatty acid linked to an elevated risk for diabetes and heart disease.

Link to information here. http://www.sciencedaily.com/releases/2014/11/141121151104.htm

The informed reader knows, serum triglycerides means blood fat or fat in the blood. Over the years many things have been stated by people going on a true low carb diet. Almost universally is a reporting of drastically reduced trigs levels. Carbs raise trig levels not saturated fat, full stop.

So, as previously stated the worst possible combination for a diabetic, looking to get non diabetic BG numbers control, is a high carb high fat diet. This sort of diet is guaranteed to raise trigs and bring about insulin resistance. Just the sort of diet the average poorly controlled diabetic is using. Hang on a minute when did the antis mention they eat a high fat diet you may be wondering. Just look at what they say they eat, they are eating more fat than they realise I reckon, and just like Gary Scheiner they struggle to get truly safe control of blood glucose levels. The NHS audited stats say 93% of type one diabetics (all insulin users) fail to get to a safe HbA1c, only to be expected when following the standard dietary advice from the NHS and the likes of Gary Scheiner, Sid Bonkers, Nobhead et al.


Above information from here. http://authoritynutrition.com/23-studies-on-low-carb-and-low-fat-diets/

Thanks for clearing that up Eddie. I knew some of that already, but not all.

The culprit of the disinformation is that most of the research of diabetes is made on rodents feed a horrible high fat diet, (not their natural diet). Also when triglycerides are measure after you eat fat you will have higher triglycerides that when you eat carbohydrates alone, that why is a very bad idea to eat high carbohydrates and fats(SAD diet or Western Diet). But what will produce a higher constant high triglycerides is a high carbohydrates diet for sure. But insulin resistance is complex and there are many theories of what causes it, many associations about what contribute to it but no generally accepted answer.

yoly wrote:The culprit of the disinformation is that most of the research of diabetes is made on rodents feed a horrible high fat diet, (not their natural diet). Also when triglycerides are measure after you eat fat you will have higher triglycerides that when you eat carbohydrates alone, that why is a very bad idea to eat high carbohydrates and fats(SAD diet or Western Diet). But what will produce a higher constant high triglycerides is a high carbohydrates diet for sure. But insulin resistance is complex and there are many theories of what causes it, many associations about what contribute to it but no generally accepted answer.

Totally agree yoly especially about the rodent studies, the anti low carb faction at DCUK have in the past oft cited them in their pathetic attempts to run down LC. I recall one were the mice on a high fat diet were fed on hydrogenated coconut oil   Even phoenix who really should know better gives credence to a rodent study on her blog in a desperate attempt to prove to herself that LC is a health risk. We know as far as LCHF rodent studies go they have never been replicated in humans nor in my mind will they ever be

graham64 wrote:

yoly wrote:The culprit of the disinformation is that most of the research of diabetes is made on rodents feed a horrible high fat diet, (not their natural diet). Also when triglycerides are measure after you eat fat you will have higher triglycerides that when you eat carbohydrates alone, that why is a very bad idea to eat high carbohydrates and fats(SAD diet or Western Diet). But what will produce a higher constant high triglycerides is a high carbohydrates diet for sure. But insulin resistance is complex and there are many theories of what causes it, many associations about what contribute to it but no generally accepted answer.

Totally agree yoly especially about the rodent studies, the anti low carb faction at DCUK have in the past oft cited them in their pathetic attempts to run down LC. I recall one were the mice on a high fat diet were fed on hydrogenated coconut oil   Even phoenix who really should know better gives credence to a rodent study on her blog in a desperate attempt to prove to herself that LC is a health risk. We know as far as LCHF rodent studies go they have never been replicated in humans nor in my mind will they ever be

Check out this bloke, this is when the cholesterol bullshit kicked off.

"In the early 1900s, a young Russian scientist named Anitschkow serendipitously conducted what would be one of the founding experiments for cardiovascular disease research. Instead of disproving his colleague’s hypothesis on ageing, Anitsckow discovered a link between cholesterol and vascular damage (atherosclerosis) after feeding rabbits purified cholesterol."

So, you stuff rabbits full of fat not exactly their natural diet, and wonder why they croak. I know it must be the PHAT!

Link to info and more here. http://blogs.scientificamerican.com/guest-blog/cholesterol-confusion-and-why-we-should-rethink-our-approach-to-statin-therapy/

Graham, I thought you said you was not going to out Bonkers and Nobhead

Rabbits never eat cholesterol so obviously they never evolved a mechanism to process it. They eat grass and their own droppings. If humans did that it would make us ill.

I hate to say it but Sid is correct - albeit in the same way a stopped clock is right twice a day.
Insulin resistance evolved as a means of food partitioning - sending fats and ketones to the tissues that prefer them and glucose to the tissues that prefer it. This works when IR takes on different values at different tissues.
Whole body IR evolved as a mechanism for the rapid storage of a glut of food as body fat. This only "works" when the IR genes are subsequently switched off and insulin levels drop to where the stored fat can be metabolised.
This is "physiological" IR, see posts from
Peter at Hyperlipid
and more in the sidebar (Peter is fearsomely knowledgeable about metabolism, but being a vet has not been correctly trained in what to ignore, unlike human doctors and researchers)
More from Stephan at Whole Health Source
who knew a lot before he became a paid up member of The Establishment

CHRONIC IR is the problem - when it is locked on it continues to store food as body fat and fails to release it.
Harry Himsworth way back in (I think) the thirties is responsible for the confusion when he found that Type 1 diabetics needed less insulin when they ate a high carb diet.
Now consider a Type 2 with Pathological (chronic) IR. To eat a high carb diet he needs a metric sh1tload of insulin. Oh, he's diabetic, he can't produce that much. BG goes up.
He eats a high carb diet. This reduces Physiological IR so he only needs half a metric sh1tload of insulin. Oh, he's diabetic, he can't produce that much either. BG goes up.
He eats a low carb diet. Pathological IR falls through the floor (trigs/HDL ratio is a good indicator). Physiological IR is now a non-factor. He CAN produce enough insulin to deal with the carbs.
This is what low carb antis and dieticians fail to understand.