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Post by sayhey24 on Dec 16, 2017 9:06:54 GMT -5
Well, whats becoming clearer and clearer as testing is getting better is more and more T2s also test positive for autoimmune. We now call them LADAs. I suspect if we tested all T2s early enough and had tests sensitive enough most T2s lost pancreatic function because of an infection which affected the beta cells. All diabetics share the same issue, they are not making enough insulin for their body's needs and all diabetics have the inability in their current condition to regenerate enough beta cells to over come their insulin shortage. Then the question is, is the attack active or not. If it is not an active attack and the beta cells are not too badly damaged we can regenerate beta cells naturally by keeping the PWD in a non-diabetic range. There has never been any evidence of beta cells regenerating (that's part of the holy grail). At best, beta cells that are dying may recover if levels are stabilized. That's what happens with the honeymoon phase in Type 1, or some of the stranger variants of Type 2 like Flatbush. However once a beta cell is dead it never regenerates. In Type 2 the problem is apoptosis. The body naturally kills and replaces cells but there can be flaws in that process. When the body kills more cells than it produces you get degenerative diseases. In Type 2 the target that is under-produced is beta cells. Don't tell Ralph DeFronzo. He 100% believes his Qatar study (not published yet) demonstrates beta cell regeneration. Al Mann in his private studies showed the same and I believe both of them. If treated early most T2 progression will be stopped and in many cases reversed. What happens in the honeymoon phase is over time the T1 is no longer keeping in a non-diabetic range and their body adapts to higher BG levels which require higher insulin levels. Whats also funny about brand new T1s is sometimes they generate near normal insulin levels and other times not as they fight the infection. The problem in most T2s is their body needs more insulin than the pancreas can make and over time their BG raises. The body adapts and wants even more insulin. Taking a walk helps by making the body use whats being made better but the root cause is not insulin sensitivity. A healthy body will adapt by making more beta cells. We know that because Ralph is showing beta cell regeneration. We also know that nondiabetic obese insulin resistant people will naturally adapt by generating huge clumps of beta cells to make more insulin. If you allow the pancreas to rest and not work over-time trying to get the BG down, in most cases it will regenerate enough beta cell function to stop progression. Today T2s are treated exactly the opposite. We promote the pancreas to work over-time by giving them metformin or some more toxic cocktail. We allow the post meal BG spike requiring even more insulin. We allow the body to adapt to higher BG overtime. And we just make a big mess of these people. |
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Post by agedhippie on Dec 16, 2017 9:25:35 GMT -5
There has never been any evidence of beta cells regenerating (that's part of the holy grail). At best, beta cells that are dying may recover if levels are stabilized. That's what happens with the honeymoon phase in Type 1, or some of the stranger variants of Type 2 like Flatbush. However once a beta cell is dead it never regenerates. In Type 2 the problem is apoptosis. The body naturally kills and replaces cells but there can be flaws in that process. When the body kills more cells than it produces you get degenerative diseases. In Type 2 the target that is under-produced is beta cells. Don't tell Ralph DeFronzo. He 100% believes his Qatar study (not published yet) demonstrates beta cell regeneration. Al Mann in his private studies showed the same and I believe both of them. If treated early most T2 progression will be stopped and in many cases reversed. What happens in the honeymoon phase is over time the T1 is no longer keeping in a non-diabetic range and their body adapts to higher BG levels which require higher insulin levels. Whats also funny about brand new T1s is sometimes they generate near normal insulin levels and other times not as they fight the infection. The problem in most T2s is their body needs more insulin than the pancreas can make and over time their BG raises. The body adapts and wants even more insulin. Taking a walk helps by making the body use whats being made better but the root cause is not insulin sensitivity. A healthy body will adapt by making more beta cells. We know that because Ralph is showing beta cell regeneration. We also know that nondiabetic obese insulin resistant people will naturally adapt by generating huge clumps of beta cells to make more insulin. If you allow the pancreas to rest and not work over-time trying to get the BG down, in most cases it will regenerate enough beta cell function to stop progression. Today T2s are treated exactly the opposite. We promote the pancreas to work over-time by giving them metformin or some more toxic cocktail. We allow the post meal BG spike requiring even more insulin. We allow the body to adapt to higher BG overtime. And we just make a big mess of these people. In the honeymoon phase you start taking insulin and your levels get under control. At that point your remaining beta cells recover and you need minimal insulin to maintain the level. However the underlying auto-immune attack is still going on and will bring you back to the previous level as your beta cells die. Illness will accelerate the process the immune system responds and as a side effect steps up the attack on the beta cells, but it's not necessary as your immune system will happily carry on killing beta cells regardless. Your control is never as good after you are ill during the honeymoon phase. I wait to see Ralph's evidence. There was nothing to suggest this in his March paper on the Qatar study. Regeneration has never been shown. Recovery yes, production of new cells even (Type 1s still make beta cells, the immune system kills them immediately though), regeneration - no. |
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Post by mnholdem on Dec 16, 2017 9:50:48 GMT -5
Somewhere, in one of these threads, I posted a link to Ralph's latest research in Texas that uses DNA therapy to transform non-beta pancreatic cells into beta-like cells that produce insulin in response to normal stimuli. Initial testing has demonstrated success in generating insulin while maintaining the cells' properties of not being attacked by the immune system like true beta cells. It could become groundbreaking therapy if successful.  |
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Post by dreamboatcruise on Dec 16, 2017 17:16:54 GMT -5
Well, whats becoming clearer and clearer as testing is getting better is more and more T2s also test positive for autoimmune. We now call them LADAs. I suspect if we tested all T2s early enough and had tests sensitive enough most T2s lost pancreatic function because of an infection which affected the beta cells. All diabetics share the same issue, they are not making enough insulin for their body's needs and all diabetics have the inability in their current condition to regenerate enough beta cells to over come their insulin shortage. Then the question is, is the attack active or not. If it is not an active attack and the beta cells are not too badly damaged we can regenerate beta cells naturally by keeping the PWD in a non-diabetic range. LADA is Type 1. It is (or was) not uncommon for someone to be initially misdiagnosed as T2 when in reality they were all along a LADA T1. As for T2, it seems there are multiple factors that can set someone down the path to becoming T2. Being overweight does lead to insulin resistance even before beta cell function starts to decline. There also seems to be a genetic factor involved for some people where they are predisposed to have beta cell function decline. It's not inconceivable that infections could play a role though I have not seen any research pointing in that direction. Some autoimmune diseases, such as the one I have, are suspected as potentially having a link to an infection confusing the immune system. I'm don't know if that is suspected for T1 diabetes. |
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Post by sayhey24 on Dec 16, 2017 19:16:50 GMT -5
So this goes back to the original question - what is a T1? If you accept the theory T2s lost pancreatic function because of a viral attack then all diabetic root cause is the immune system killing off the beta cells. The genetic factor is two fold; how fast can their body regenerate beta cells; and their genetic insulin sensitivity.
20 years ago ALL LADAs would be T2s. Today we test more because NOBODY wants to be called a T2 because of the social stigma that they have diabetes because they are fat, lazy and ate too much. If we tested more and sooner we would have even more LADAs or some new term. How many MODYs do we have now 14? Almost everyone I talk with thinks they got T2 because they ate too much. My Dad thought he got it because he use to have a 12 ounce glass of Coca-Cola with his lunch. Nobody wants to be a T2, the social stigma is too high. Some people have LADA parties when they find out it was not their fault they got diabetes.
60 years ago we had insulin dependent and non-insulin dependent. There was no T1 and T2. Then came UpJohn and Orinase who invented the terms T1/T2 for marketing purposes to sell their Orinase. The sad thing is UpJohn knew in the 1950's that the best approach was early insulin intervention but that sure was not going to sell their new blockbuster. At least Orinase was finally pulled from the market after it did so much damage but UpJohn left us the terms T1 and T2. T2s are those BP can push their toxic, expensive non-insulin products to until their pancreas wear out and then they are "Insulin Dependent". The last thing BP wants is the T2 using a CGM and knowing their numbers.
The real main difference between a T1 and T2 is how much insulin are they currently making and do they have an active autoimmune attack. For those who are not under current attack the question is how much beta cell functionality do they have left. Diabetes is really better defined by degree of beta cell function not by class.
Now to clear up a common misconceptionabout being fat and lazy - Being overweight does lead to insulin resistance even before beta cell function starts to decline BUT who cares. In a healthy non-diabetic their body will adapt and will naturally generate more beta cells and make more insulin to counteract the insulin resistance. All you have to do is autopsy an insulin resistant nondiabetic and you will see the big clumps of beta cells. Being insulin resistant is not the cause of the diabetes but contributes to the person recovering after an attack because they need more insulin than their pancreas can now make. BG then rises and they need even more as the pancreas works overtime and finally gets worn out.
To help them recover after the attack you can have them take a walk and become more insulin sensitive but in most cases its simply not enough. This is why DeFronzo is succeeding with his Qatar study. He is able to keep the PWD in non-diabetic range and is reducing the post meal spike by use of the GLP-1.
However, the best thing to do is have them take the walk and have them take afrezza at the same time. This should fix up most without using toxic drugs. Afrezza is basically the natural approach to healing the pancreas.
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Post by mango on Dec 16, 2017 22:13:07 GMT -5
It all comes down to a dysregulation in homeostasis.
Even the autoimmune response is caused by a deficiency/dysfunction in endocannabinoid tone, an imbalance in homeostasis/an homeostatic dysfunction—and the CB2 receptor regulates immune cells.
The ECS regulates glucose homeostasis, insulin secretion, brain glucose homeostasis—all energy homeostasis, etc...—it's the body's homeostatic regulatory system.
Afrezza restores the first-phase insulin response. The first-phase insulin response is a key player in the regulation of glucose homeostasis. Dysfunction or loss of the first-phase insulin response=dysregulation in glucose homeostasis.
Homeostasis=a state of balance to maintain health
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