Discussion Board

I was reading studies on Pubmed that has recently changed my mind on insulin-resistance. According to numerous studies, diabetes is caused by a condition called “lipotoxicity”. I’m not going to post the numerous studies that prove this… it would be far too tedious, but I assure you the science is there.

Basically the adipose-tissue (body-fat) can only store so much dietary-fat. Insulin shuttles fat you eat into adipose-tissue and prevents adipose-tissue from releasing free-fatty-acids (it prevents fat breakdown) called lipolysis. The more fat that is stuffed into the adipose-tissue, the larger the fat-cells expand and the less sensitive they become to insulin. Eventually a point is reached where the adipose-tissue becomes resistant to the actions of insulin (due to being over stuffed with fat). When the adipose-tissue becomes insulin-resistant, insulin can no longer inhibit lipolysis.

Increased lipolysis sends free-fatty-acids into the bloodstream (causing atherosclerosis) and they accumulate thought the body causing fatty-heart, fatty-liver and fatty-muscles. The accumulation of fat on these organs inhibits the ability of insulin to promote uptake of nutrients in these tissues and they literally began to starve to death. Excess free-fatty-acids also accumulate on the pancreas and impair insulin-secretion.

Interestingly enough, studies show that fasting causes an increase in liver-fat, muscle-fat and intramyocelluar-lipid accumulation, due to decreased insulin-secretion and increased lipolysis. This also explains why moderate alcohol consumption promotes health and decreases the risk of metabolic-syndrome; alcohol is metabolized into acetate, which is a potent inhibitor of lipolysis [1]. However too much alcohol decreases appetite, decreased appetite means less insulin-secretion, leading to increased lipolysis and therefore fatty-liver… commonly seen in alcoholics.

The solution to all of this would be to eat foods that cause insulin-secretion (to inhibit lipolysis) and foods that are naturally low in fat (to prevent adipose-tissue from being overstuffed with fat). Starches fit the bill perfectly. Fruit not so much, because most of the calories in fruit (or sugar in general) is fructose, which actually converts into fat in the liver and does not stimulate insulin-secretion. Starch is pure glucose, which does not convert into fat, and effectively stimulates insulin-secretion.







[1] Am J Clin Nutr. 1999 Nov;70(5):928-36. De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption. Siler SQ, Neese RA, Hellerstein MK.

very interesting...certainly supports the importance of keeping your weight down and not overeating.

Since I have some kind of diabetes (not overweight, but I think there might be some insulin resistance playing a part) I'm interested in anything out there that would increase insulin resistance. That includes too much fructose.

As others have posted, I, too, wonder about incrurring long-term damage from sugar spikes; this happens with potatoes and more than about 1 c (cooked measure) of whole grains.

Has this changed your choice of what you eat?

Maer

Has your expanded viewpoint changed your thoughts on intermittent fasting? While increased lipolysis sends fatty acids through the bloodstream, doesn't it do so during fasting periods for the fats to be oxidized and burned as energy (as also happens during fed states), and not to be deposited in places where fats shouldn't accumulate?

Insulin spikes are actually good. Insulin does amazing things in the body, such as building muscle, increasing nitric-oxide, building bone, transporting minerals into cells, suppresses free-fatty-acids, increases testosterone production and much more. However if fat is present with insulin (baked potatoes with butter), the fat is going to be stored, and if you store too much fat, it can spill out of the adipose-tissue and end up in the muscles or liver and cause metabolic-syndrome.

For a person with low body-fat or people trying to build muscle, high-glycemic starches are ideal, foods like: flour, white-rice, potatoes, grits are perfect for building muscle, however they inhibit lipolysis much more than low-glycemic foods, which will drastically slow or halt fat-loss. Obese people or persons with diabetes need low-glycemic starches like barley, oats, pasta, beans, sweet-potatoes… once they have lost an appropriate amount of weight, then they can begin to eat high-glycemic starch.

Both fat and sugar (fructose) is what causes insulin-resistance and obesity. Overeating starch actually builds muscle and overeating fat and sugar builds body-fat [1].

I am very underweight, always have been even on a high-fat/high-sugar western-diet. In order to build muscle and put on weight I now overeat on high-glycemic starch and do resistance training.




[1] http://veganmaster.blogspot.com/

Yes. Fasting (starvation) shares the same metabolic-pathways as diabetes.






During fasting or starvation, free-fatty-acids are released during lipolysis into the liver and muscles to be burned as energy, this is called fat-oxidation. During the fed-state and especially while eating a starch-based-diet, fat-oxidation is inhibited and replaced with carbohydrate-oxidation, insulin is what mediates this shift. When carbohydrate-oxidation is taking place, fatty-acids are shuttled back and "locked away" in adipose-tissue... where they belong.

In diabetes, insulin cannot shuttle the glucose into the cells (therefore carbohydrate-oxidation is inhibited) and the body has no other choice but to undergo lipolysis and start burning free-fatty-acids. Depending on how much body-fat you have and the types of fatty-acids that your body-fat consists of, determines the "flux" of free-fatty-acids to ectopic-sites in the body. Too much "flux" and not enough oxidation causes lipotoxicity.

Wow thats a lot of big words and science for a friday. Let's see if we can simplify it:

Follow the McDougall Plan

That about covers it, right?

If this were true, then why is fat still oxidized during the fed state? The body burns a mixture of fuels at all times, does it not? And while, yes, the fed state may not up regulate body fat oxidation like a fasted state may, is the up regulation of the release of stored fat into the bloodstream during a fasted state necessarily harmful considering these fats are being burned, and not stored?

Very interesting, Mr. E., and while we may not understand all of it...we can eat our unrefined starches to prevent or reverse DM!!!

The body does burn a mixture of fuels at all times, but the ratio is drastically different in fed/fasted states.



That is a good question; I don't think anyone knows exactly. I do know that increased lipolysis (due to decreased insulin-sensitivity in adipose-tissue) is probably the underlying cause of metabolic-syndrome. However this increase in lipolysis happens in the fed-state with diabetes, in which normally it would be inhibited.

It is sort of a catch-22 situation: eat more starch and store fat in adipose-tissue instead of ectopic-sites (liver, muscles, heart) or fast and have a decrease in adipose-tissue but more fat exported to ectopic-sites.

Same could be said for the Atkins-diet: are the fats necessarily harmful considering these fats are being burned, and not stored? So far the evidence suggests yes. When you fast, free-fatty-acids dramatically increase [1]. Same happens with the Atkins-diet [2]. Atkins has even said before, that his diet primarily works the same way as fasting.




[1] Clin Sci. 2008 Apr;114(8):543-5. Is adipose tissue lipolysis always an adaptive response to starvation?: implications for non-alcoholic fatty liver disease. Gan SK, Watts GF.

[2] J Am Diet Assoc. 1980 Sep;77(3):264-70 Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. Larosa JC.

On the Atkins diet, initial weight loss is water. The diet is dehydrating. When starches are added back, the carbs store water. Atkins dieters lose weight because they are on fewer calories, just like any other weight loss diet. The ketosis does abate hunger which is probably why people eat fewer calories.

The Atkins diet will work for a while for diabetics but Atkins acknowledges that people "adjust" (his word) to his diet and start to spill sugar again. So he invented the meat and millet diet using about 150 grams of starchy carbs (not just millet). I think they "adjust" because the Atkins diet, in the long run, makes diabetics even more insulin resistant.

If fat is stored in the muscles on a high starch diet then how come so many people lose weight on a high carb diet? And if fat is stored in the liver, how come the liver numbers become normal which can be shown on a blood test, and those with fatty liver actually find that the fatty liver can be reversed?

I don't know if I am understanding this. If lipolysis is the breakdown of fats in the cells then how can that cause metabolic syndrome? One is insulin resistant because insulin can't get the sugar into the cells because the fat in the cells prevent it. And probably eating fat also prevents the insulin from "unlocking" the gate that lets the sugar into the cells.

Didi

I ask these questions for intelligent discussion, as the matter has confused me for some time as well.
Of note on the Atkins diet, fat intake often exceeds the rate at which they can be burned, and being a higher percentage of calories from fat, whether hypocaloric or in calorie balance, the total calories of fat deposited into fat cells far exceeds the rate at which occurs on a high carb low fat diet.
To me it seems counter intuitive that going without food enable a disease like type 2, when in fact there is evidence that calorie restriction and fasting is beneficial.
It would also make little sense to me that the physiologically healthy release of fat into the bloodstream, such as in cases of weight loss, calorie restriction, or intermittent fasting, would support a disease like Type 2 diabetes. The release of fat is just a transport. Where the fat goes, and what the body does with it, is ultimately more important, if not the only thing that matters.

I feel that while lipolysis indeed plays a role in Type 2, it is just one of many parts of the bodywide dysfunction that is diabetes, and to say that because a disorder involving the malfunction of lipolysis is cause for concern in regiments involving non disordered lipolysis, such as weight loss or intermittent fasting, is a bit of a stretch.

My thoughts anyways.

On a high-starch diet the fat is stored in the adipose-tissue not the muscle or liver. On the high-fat Atkins-diet or while fasting the fat is floating free in the bloodstream and accumulated in the muscles, liver, heart and elsewhere. This gives the illusion that you are thin and healthy, when in fact you are fatty. My research has led me to believe that fat needs to be stored in the adipose-tissue.




The breakdown of body-fat (adipose-tissue) releases a huge amount of free-fatty-acids into the bloodstream, these free-fatty-acids then accumulate in non-adipose-tissues like the muscles or liver and block the ability of insulin to work properly. Eating starch (and stimulating insulin-secretion) shuttles these free-fatty-acids back into the adipose-tissue where they belongs.

The thing is thou, on the Atkins-diet, fat is never transported into the adipose-tissue, it either floats in the blood or accumulates in ectopic-sites, due to the lack of insulin-secretion.



Actually studies show that during starvation and prolonged-fasting you actually become insulin-resistant, due to increases in free-fatty-acids and cortisol. Studies also show that rapid-weight-loss, prolonged-fasting and ketogenic-diets can actually induce NAFLD (non alcoholic fatty liver disease).

fat stores itself incredibly well with our without insulin. Research acylation-stimulating protein (ASP).



But does the temporary insulin resistance in the wake of increased, IF (16-8, or 20/4) related lipolysis cause or become indicative of the permanent damage to insulin receptors as seen in type 2???? I just can not see, nor have I found, anything that points to "not eating" causing type 2, and you yourself have even said that intermittent fasting increases insulin sensitivity, or at least decreases insulin resistance where it is already present.

"Intermittent Fasting does not effect whole-body glucose, lipid, or protein metabolism"
http://www.ncbi.nlm.nih.gov/pubmed/19776143

Amylin is co-secreted with insulin in non-diabetics. amylin has appetite suppressant and lipolytic effects. It is not as simple as "eat carbs, plug up your fat burning machine."

Here's a really good series about this sort of this: http://weightology.net/weightologyweekly/?page_id=319