Fat causes insulin resistance?

#1

Can anyone comment on the below, that I was directed to?

If this has been dealt with elsewhere, please feel free to point me in that direction. Thanks…

(Jon Barclay) #2

This makes no sense. If this hypothesis that fat caused insulin resistance were true, and that lowering dietary fat would increase insulin sensitivity, we would be curing type 2 diabetes with low fat diets. In fact it’s ketogenic diets that get people off insulin and diabetic medications.

#3

Agreed, but I’m interesting in a scientific response.

These are two discussions I have been able to find…

Because the muscle tissues become more adept at using BHB, GLUT receptors are down-regulated at the muscle level as a person becomes more keto-adapted. Although we still have much to learn about the keto-adapted state, we know that this occurs more prominently in the muscle tissues than in the gut and brain. This fascinating glucose sparing phenomenon, has been interpreted by some as “worsening insulin resistance.”

Going very low carb – to around or below 10% of calories, or full-blown ketogenic – can induce “physiological” insulin resistance. Physiological insulin resistance is an adaptation, a normal biological reaction to a lack of dietary glucose. As I’ve said in the past, the brain must have glucose. It can use ketones and lactate quite effectively, thus reducing the glucose requirement, but at the end of the day it still requires a portion of glucose. Now, in a low-glucose state, where the body senses that dietary glucose might not be coming anytime soon, peripheral insulin resistance is triggered. This prevents the muscles from taking up “precious” glucose that the brain requires. The brain’s sensitivity to insulin is preserved, allowing it to grab what glucose it needs from the paltry – but sufficient – levels available to it.

Have the keto experts talked about negative effects of "intramyocellular lipids" (IMCLs)
#4

I dare say the folk currently at Breckenridge would have a bit to say about this, together with some good counter articles. @richard, @carl, @Brenda and co…can any of you assist with this query, please?

(Todd Allen) #5

As someone who spent decades as either vegetarian or vegan and still eats a lot of plant foods since going keto I have a bottomless black pit of contempt for Dr. Michael Greger. He is a proselytizing vegan zealot on a mission and cherry picking nutrition “science” is his method. One can get a sense of the dismal state of nutrition science from Nina Teicholz, Gary Taubes and many others. Nutritional studies flout established principles of scientific practice and produce endless amounts of conflicting interpretations ripe for cherry picking.

Anyway, regarding carbs, fat and insulin resistance my understanding of it is definitely incomplete and likely with some degree of misconception but I’ll share it anyway to provoke discussion and explain why I think Dr. Greger is full of sh*t on this subject.

First there are several different ways insulin resistance is measured and they don’t give the same result because they aren’t measuring exactly the same thing. And one can find differing definitions of the term nsulin resistance as well. But loosely insulin resistance is a loss of ability to regulate blood sugar. Our ability to regulate blood sugar depends on a large number of factors both short and long term.

We tend to a state of either predominately burning glucose or fat for energy which is largely controlled by the amount of carbohydrates consumed. The more time we spend burning fat for energy, ie the more fat adapted we are the more short term factors of glucose metabolism are down regulated. The body won’t waste a lot of amino acids and energy maintaining high levels of enzymes involved with glucose metabolism when it doesn’t need them. This is why it is recommended for people eating keto to transition back to a higher carb diet for several days prior to taking an OGTT or other test of insulin resistance.

Long term factors are responsible for the damaging insulin resistance leading to type 2 diabetes. In the presence of a high carb diet and high insulin, dietary fat is mostly stored and not burned and may contribute to increasing insulin resistance by increasing obesity. There is substantial evidence carb induced chronically elevated insulin is a big factor in weakening the signaling effect of insulin and is reversed by a keto diet. A weight losing keto diet that reduces visceral fat can improve the functioning of the liver and other organs with benefits for glucose metabolism beyond improved insulin signaling.

The studies Dr. Greger looks at fail to filter out the relatively unimportant short term impacts of a high fat diet and don’t separate and accurately attribute the long term consequences of high carbs with varying levels of fat consumption.

#6

I saw no mention of the level of carbs the high fat group was eating. I’m willing to bet they were not ketogenic.

Also, this part is false:

Insulin is the key that unlocks the door to let the glucose in the blood to enter the muscle cell. So insulin is the key that unlocks the door into our muscle cells.

Muscle cells can take up glucose via transporters that are not insulin dependant. Insulin just adds more.
Fat cells, on the other hand, need insulin to store fat. It is the fat cells inability to expand that causes the insulin resistance.

(Gabor Erdosi) #7

My take on insulin resistance (IR).
First of all, don’t confuse acute or physiological IR with chronic IR. The latter is what most think of when talking about IR. Chronic IR is caused by sustained elevation of insulin. More precisely by fat accumulation in fat cells. Even more precisely, by the way how fat accumulates in fat cells. Overly enlarged (hypertrophic) fat cells are insulin resistant, meaning that they are unable to take up glucose via GLUT4 transporters, and this impairs glyceroneogenesis and de-novo lipogenesis. This practically results in reduced fat uptake after meals. At the same time, these cells leak free fatty acids (FFA), so higher insulin is necessary to achieve adequate FFA outflow at tissue level. The degree of insulin resistance can be described as the proportion of hypertrophic fat cells to normal ones.

(Stickin' with mammoth) #8

Well, slap me with bacon, you just described every vegan I’ve ever met in Portland, Oregon! (Including me, three years ago. I was so young.)

This seems to be a preferred technique among that crowd. What baffles me is when they use people who aren’t in ketosis yet to prove ketosis doesn’t work. That’s like pointing to a teen-aged girl and saying, “See? Menopause is a myth.”

(8 year Ketogenic Veteran) #9

Show me the science Forks Over Knives!

(Matt Meeks) #10

Anyone here heard of this “documentary”: http://ithriveseries.com? I was mislead a bit into starting to watch it, and I’m shocked at the amount of pseudo-science, unsupported claims, and outright falsehoods presented by people with M.D. or PhD after their name. I had to stop watching it-some of the “experts” were making pretty wild claims like a ketogenic diet would cause cholesterol to go up (mine has dropped by over 150 since starting keto), that fat causes blood sugar to spike, but things like potatoes, rice, beans and pasta do not, and that carbs from those kinds of foods are somehow completely different than carbs from processed foods, in spite of the fact that the science says different.