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Meat, Eggs, and Insulin Resistance


according to the insulin index, eggs and meat raise insulin by quite a large amount. so if we were to eat high protein via eggs and meat throughout the day, we would have high insulin throughout the day.

high insulin leads to insulin resistance, diabetes, getting fat, etc. though it seems like high protein/fat/low carb diets including eggs and meat improve sensitivity, reduce the risk of diabetes and helps in cutting. what gives?


high insulinemia doesn't mean high glycemia. Eggs/meat still have a low GI. The rise in insulin is good because it helps drive amino acids into the muscle cells, since insulin stores nutrients.


Well, protein does raise insulin levels, but protein also raises the hormone glucagon.

Dr. Eades had a nice write up about the two hormones use in the body recently.

"Why We Get Fat"

From the article:

"Some people with a little learning may be quick to point out that protein drives insulin up as well. This is true, but with a catch. Protein drives both insulin and glucagon up, so you don?t have the pure insulin effect. Only carbs will give you that. With carbs, insulin goes up while glucagon goes down. With meat and other proteins, the effects of the elevated insulin are muted by the concomitant rise in glucagon. (Glucagon isn?t called insulin?s counter-regulatory hormone for nothing.)"


thanks. does insulin also promote fatty acid absorption in all cells via some transport? if so, is the fat we eat digested, turned into fatty acid, then put in the bloodstream (making the fat available to cells), and does it have any preference for muscle/adipose/liver cells?


high insulin doesn't lead to getting fat. Eating more calories than you're burning leads to getting fat.

Fat is always digested and first stored in fat cells, and then the fatty acids can be released to be burned. Fat cells can be located in a variety fo areas, regular subcutaneous fat, fat in muscles (often associated with trained athletes), and fat in the liver (generally bad). In fact, we want the fat to be digested and stored in the fat cells, because otherwise we have triglycerides or free fatty acids floating around in the bloodstream, which is a symtom of metabolic syndrome.


As far as I am aware, insulin does not stimulate fatty acid absorption in any cells (at least short term like it can with glucose). Some cells (adipose) begin producing more enzymes that break down the fats in the blood for absorption into the cell after constant insulin stimuli. But this still isn't a preference occurrence; the fat cells just begin to collect more than they normally would.

Like you said, the fats circulate in the blood - but at the core of lipoproteins, as triglycerides. The lipoproteins circulate and release fats when they react with those enzymes I spoke about earlier. The place where the fats end up would be split between muscle, adipose, liver etc - But the split would likely be influenced by many factors, like mass of tissue, microvascular density, metabolic activity of tissue and influence of cyto-, adipo- and chemo-kines.


so the fat we eat is never digested first for energy; it is stored in fat cells, then released if needed and then burned? sounds very inefficient
and having FFA in bloodstream is a sign of a health problem? i thought FFA needs to be in the bloodstream in order for it to be burned by cell (since you mentioned 'released')


No. Fat (found as triglycerides in food) is broken down to free fatty acids inside the small intestine. These are then repacked as triglycerides inside lipoproteins and secreted from the intestine (enterocytes). These fats then circulate to be distributed around the body.

Fat can be stored in fat cells. It is released from fat cells as free fatty acids. These are NOT the major source of fats as fuel. The liver takes up a lot of fat (free fatty acids and fat from lipoproteins), repackages them as VLDL (large, fatty version of LDL) and secretes them into blood.

So the major source of fat for fuel comes from lipoproteins (intestinal or hepatic).
Free fatty acids can be released in abnormally large amounts when adipose tissue is inflamed.


thanks for the info, took a little bit of time to grasp that.
you say that fatty acids from fat cells are NOT a major source of fats as fuel, and that liver FFA and lipoproteins, which turn into VLDL that move into the blood, is the major source of fuel. if so, how do people lose fat then?

when the body burns fat for fuel from lipoproteins, what exactly happens -- do they just spontaneously release energy or need to go to the liver for a biological process?

lastly, how can you get adipose tissue inflamed (im assuming large amounts of released FFA is good to promote fat loss?)


Think of it like this: when fat is absorbed by the body, it is always in the body until it is burned - no matter where in the body it is. Adipose tissues function is to store the fat, which is does quite well. When the body is in 'fat balance' the release of fat from adipose equals the amount taken up (from lipoproteins). Some of the fat released from adipose makes it to the liver, where it goes into the synthesis of VLDL. The faster the adipose releases fat, the quicker VLDL is formed. VLDL is only released once it is completely formed. The VLDL travel in the blood vessels around the body where cells can use them to take up fat (including adipose tissue). A cell takes up the fat and can oxidise it for fuel/energy.

If the person is in negative fat balance, adipose releases more fatty acids than it takes up - the person loses fat. So, it is important to consider both the uptake and release of fat from adipose tissue when talking about fat loss. Supplements that just increase fat breakdown move the fats into the blood, where it is likely to come straight back (same as inflammation).

Cells can use free fatty acids for fuel. The problem is that little regulation occurs as to which cells receive the fat. Normally, lipoprotein lipase (enzyme is spoke of earlier) is expressed on cells with a high metabolism, so they can most of the fats. Free fatty acids can just move into any cell. Once inside, it can even produce toxic substances under the right conditions.

Adipose tissue inflammation can be described in two ways: 1. oversupply of fats which hypertrophy adipose cells to the point where they become de-regulated. 2. infiltration of macrophages followed by activation to their inflammatory state (think low grade whole body inflammatory state). The exact causes can be numerous, but it definitely is not a good thing.


wow that is a very clear explanation, thanks for your time to type that all up.

you said adipose releases fat and some travels to the liver, which creates vldl. only vldl? since hdl is good, ldl is bad, i figure vldl is very bad!

how did you get so much into the science of nutrition in the first place?


VLDL = Very low density lipoprotein; LDL = Low density lipoprotein; HDL = High density lipoprotein.
They are obviously based on their density :stuck_out_tongue: But their composition dictates their density. So lipoproteins that have lots of triglycerides are the least dense (VLDL and chylomicrons); those with little triglycerides and lots of cholesterol are very dense (HDL and LDL).

VLDL is slowly sucked dry of its triglycerides and gradually turns into LDL. Large, low density particles are considered to have no ill effect on the body. Small, dense particles have the potential to have deleterious effects. However, HDL is composed quite differently and so has unique, beneficial functions.

In a nut shell, lipoproteins only become atherogenic once their composition is abnormally altered for some reason (being in the blood for too long for instance). High LDL cholesterol is just one marker used which 'may' suggest that some of these changes are occurring.

I originally studied nanotechnology but changed to nutrition. I then got fed up with the direction the dietetics department was heading, so headed down nutrition science. I am currently researching the role of nutrition in dementia and vascular biology.


What evidence do you have to support this assertion?

If I recall correctly, the insulin response from meat/protein is monophasic, only stored insulin is released. Carbohydrates illicit a biphasic response, where stored insulin is released and then more insulin is produced by the pancreas, which is going to be far more likely to cause insulin resistance.


I seriously recommend locking this thread (and similar ones) if the phrase 'insulin sensitivity' pops up again...