Of course, choline deficiency and a high intake of fructose and vegetable oil (how a lot of Americans eat) is going to exacerbate a fatty liver also.
Last edited by Timthetaco; 10-17-2013 at 01:13 PM.
I think- wrong. First of all, T2 diabetes *usually* means that pancreas is still potent enough to produce adequate amonut of insulin. It's the insulin resistance that is the bad guy. Second of all- I think that, like in all the other chronic diseases, what we should be mainly worried about are the complications and long-term effects- in this case, excess glycation and all its deadly effects.
If a low-carb diet can get one's BFG to NORMAL and HBA1c to healthy range- by improving insulin resistance- most likely that person should not be worried about the consequences of diabetes he'd otherwise would have to face. I think that's what matters- especially as we're facing T2 diabetes epidemic now.
Steve Cooksey did well on a (self-administered) OGGT, and he was so excited about the results he decided to stay very low carb for the rest of his life, unnecessarily. To each their own.
T1DM ( insulin dependent ) is an autoimmune disease in which the body attacks the beta cells of the pancreas, eventually, there are very few active cells left, and the individual is left incapable of producing insulin. This type of diabetes used to bear the name "juvenile diabetes" because being an autoimmune disease it would present early in life.
T2DM ( non-insulin dependent diabetes ) is a condition where the pancreas secretes more than enough insulin, but the body does not respond to insulin signalling. When the body becomes insulin resistant, this represents saturation of the largest energy sink that the the body possesses ... adipose tissue. Once adipose tissue can no longer assimilate nutrients, they remain in the distribution network : the circulatory system. Now, saturation of fat cells does not imply morbid obesity. Rather, it means that that particular individual has gotten as fat as they can. Depending on the underlying musculature, and the number and distribution of fat cells of the individual, they may not look particularly overweight. The caveat here is that our notion of what an overweight individual looks like is a moving target, and your average 30ish North American male is walking about with a body fat percentage in the mid 20s.
Your claim that you cannot assimilate calories if you have T2DM, and that this make those calories "not count" is ludicrous. The quickest, most effective way to remedy T2DM is to restore capacity to your adipose tissue. The way to do that is to draw down the contents of fat cells, and the quickest way to that is to not eat, to fast. The calorie that doesn't count is the one you don't put in your mouth. Otherwise, they all count.
Thank you for the contributions here.
A1c changes drastically in short order due to diet. An A1c number is used to determine if someone has Type 2 Diabetes, but simply avoiding carbohydrate for 2 or 3 weeks will lower your A1c number low enough to where you won't qualify as a Type 2 Diabetic. However, you've cured nothing, you've just removed sugar from your bloodstream. You still can't process it.
Don't put your trust in anyone on this forum, including me. You are the key to your own success.
That is (and you alluded to it) that in IR and T2 diabetics the release of insulin is delayed and slow to rise. That is the cause, everything else we see is a result of that. Postprandialy glucose and fatty acid uptake in the liver, muscle and adipose tissue is blunted because of the still high glucagon and low insulin levels. Because glucagon is still high, glucose and fatty acids are still being released ONTOP of the already high post prandial serum levels of both substrates. Metformin is taken to counteract post prandial glucagon secretion.
When insulin levels finally rise (as you said the pancreas is still capable of high amounts of insulin release, Just that it is slow to rise and is delayed) the T2 diabetic respond normally to insulin. Filling its cells with the energy substrates circulating in the serum as a normal person would. This can be seen with insulin injections as well, they work quite fast, the body don't seem to have trouble processing insulin when injected intravenously.
So this is what I think IR and T2 diabetes is caused by; the signaling mechanism that "detects" serum glucose levels becomes progressively "resistant" to the high & prolonged levels of glucose in the blood. This causes a delayed and slowed insulin reaction, every symptom we see happens from here. Even tho the pancreas is still capable of 100% capacity it is not receiving the correct signal to release the appropriate amount of insulin. The body cells still have 100% insulin sensitivity when it finally arrives, just there is no insulin in the blood for our cells to be sensitive to for a while post prandialy.
The reason a low carb diet is effective in the control of IR and diabetes is that the body is running glucagon Postprandialy anyway, might as well feed it substrates that glucagon works to break down like proteins and fats. This also gives your BG detector time to become more sensitive to changes in BG. Reduce the so called "resistance" to insulin.
Last edited by dilberryhoundog; 10-17-2013 at 10:36 PM.
A little primal gem - My Success Story
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