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Post by digger on Oct 26, 2017 23:00:30 GMT -5
IMO this is a very flawed study. Allowing the afrezza arm to administer insulin as much as they need to post meals doesn't make sense. Of course you will see better "time in range" when that group is allowed to continually admin insulin. The injectable group only does it once prior to their meal so why not same restriction with afrezza group? There is a reason for that. Afrezza is an insulin you can take. with out it killing you. afrezza allows for better after meal blood glucose control.
If the study allowed the subq rapid acting analog post meal insulin to control post meal spike, they would die. Subq RAA the diabetic, goes high, then low.
Why would treating hyperglycemia with an injectable after a meal be any different than treating hyperglycemia any other time? I imagine diabetics often have occasion to inject themselves between meals to treat elevated sugars. Also, isn't there a risk that the study will demonstrate that supplemental afrezza dosing is actually necessary to control PPGE, etc, in afrezza users? That might not be looked upon very favorably. |
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Post by rockstarrick on Oct 26, 2017 23:58:07 GMT -5
IMO this is a very flawed study. Allowing the afrezza arm to administer insulin as much as they need to post meals doesn't make sense. Of course you will see better "time in range" when that group is allowed to continually admin insulin. The injectable group only does it once prior to their meal so why not same restriction with afrezza group? Ok, I’ll give it a try,,, the reason the injectible group only “does it once” is because the current Injectible Mealtime Insulin options stay in your system longer than it takes to digest a meal, this makes stacking Insulin for better blood glucose extremely dangerous. The reason the Afrezza group takes follow up doses, is because they can !! I’m quite sure there are lots of times when a PWD would like to take a follow up dose of injected RAA because of a miscalculation, but the time stamp of the product doesn’t allow them to safely do it, You wouldn’t wind up with a better glucose reading if you stacked an injectible RAA, you’d most likely wind up in the hospital or dead 💀 if this was even remotely possible, PWD would’ve been doing it. Watch and learn sonny boy, times are changing, There’s a New Sheriff in Town !! Read em and weep,,,, Afrezza Made in America 🇺🇸 |
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Post by mango on Oct 27, 2017 5:09:57 GMT -5
Also, isn't there a risk that the study will demonstrate that supplemental afrezza dosing is actually necessary to control PPGE, etc, in afrezza users? That might not be looked upon very favorably. Think about what you basically just implied here. Who would be the ones seeing supplemental dosing with Afrezza as something unfavorable? The non-diabetic physicians who don't have to take insulin daily or the people with diabetes that do? A supplemental Afrezza dose isn't even close to what treatment burden is so it couldn't be that. A supplemental dose isn't going to cause a hypo so it can't be that either. I wonder what could possibly make someone view the tight regulation of blood sugar as being unfavorable? Maybe you can tell me. Postprandial glucose becomes increasingly more significant and eventually becomes the dominating contributor of A1C when the A1C is <7.3%. PPG also contributes at least 50% of A1C when the A1C is <8.4%. What might be seen as unfavorable, at least in my mind, would be the people that still thought postprandial glucose homeostasis wasn't important and that the Standards of Care shouldn't become illegal. |
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Post by sayhey24 on Oct 27, 2017 5:33:55 GMT -5
There is a reason for that. Afrezza is an insulin you can take. with out it killing you. afrezza allows for better after meal blood glucose control.
If the study allowed the subq rapid acting analog post meal insulin to control post meal spike, they would die. Subq RAA the diabetic, goes high, then low.
Why would treating hyperglycemia with an injectable after a meal be any different than treating hyperglycemia any other time? I imagine diabetics often have occasion to inject themselves between meals to treat elevated sugars. Also, isn't there a risk that the study will demonstrate that supplemental afrezza dosing is actually necessary to control PPGE, etc, in afrezza users? That might not be looked upon very favorably. What the 171 study showed us was most afrezza users did not supplemental dose and the PWDs A1c was about the same as RAAs. In the case of one doctor it was shown his PWDs did supplemental dose and his numbers where so good the FDA accused him of cheating. Supplemental dosing gives the PWD the option of how good do they want their numbers. If they want near non-diabetic numbers they have that option. If they want A1c about what they have today, then one puff will do it. However, to win the A1c challenge in the study all PWDs should be checking one and two hours after eating and take whatever is needed to get <90. Its always nice to have options and thats what afrezza provides. If BP wants to paint that as unfavorable, I can't blame them because if afrezza takes off as Al Mann thought, it will obsolete the entire T2 product market and kill most of the current RAA and basal market. Listen to this guy he does everything possible not to have his PWDs take insulin because its too dangerous for them in his option. vimeo.com/222254561 Meanwhile he will give his PWDs a cocktail of potentially toxic drugs which have been shown to cause all kinds of issues from amputations to pancreatic cancer. Now that is something I find unfavorable. |
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Post by liane on Oct 27, 2017 5:49:26 GMT -5
sayhey24 - your link is not to the specific page.
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Post by mnholdem on Oct 27, 2017 7:24:10 GMT -5
Dr. DeFronzo could be pushing his message about the dangers of taking insulin because he is a co-inventor of a new gene transfer therapy that causes other cells to produce insulin in response to glucose, which would replace damaged, non-insulin producing pancreatic beta cells of patients with Type 1 diabetes.
Source: news.uthscsa.edu/diabetes-breakthrough-increases-insulin-producing-cells/
Excerpts:
A potential cure for Type 1 diabetes looms on the horizon in San Antonio, and the novel approach would also allow Type 2 diabetics to stop insulin shots.
The discovery, made at UT Health San Antonio, increases the types of pancreatic cells that secrete insulin. Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes at UT Health, is co-inventor on the patent. He described the therapy:
“The pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],” he said. “This is basically just like beta cells.”
Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn’t use insulin efficiently.
The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin. Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body’s immune defenses.
“If a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” Dr. DeFronzo said.
The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored. “A major problem we have in the field of Type 1 diabetes is hypoglycemia (low blood sugar),” Dr. Doiron said. “The gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.” People don’t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said.
“We don’t need to replicate all of the insulin-making function of beta cells,” he said. “Only 20 percent restoration of this capacity is sufficient for a cure of Type 1.”
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Post by mango on Oct 27, 2017 7:38:59 GMT -5
Dr. DeFronzo could be pushing his message about the dangers of taking insulin because he is a co-inventor of a new gene transfer therapy that causes other cells to produce insulin in response to glucose, which would replace damaged, non-insulin producing pancreatic beta cells of patients with Type 1 diabetes.
Source: news.uthscsa.edu/diabetes-breakthrough-increases-insulin-producing-cells/
Excerpts:
A potential cure for Type 1 diabetes looms on the horizon in San Antonio, and the novel approach would also allow Type 2 diabetics to stop insulin shots.
The discovery, made at UT Health San Antonio, increases the types of pancreatic cells that secrete insulin. Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes at UT Health, is co-inventor on the patent. He described the therapy:
“The pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],” he said. “This is basically just like beta cells.”
Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn’t use insulin efficiently.
The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin. Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body’s immune defenses.
“If a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” Dr. DeFronzo said.
The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored. “A major problem we have in the field of Type 1 diabetes is hypoglycemia (low blood sugar),” Dr. Doiron said. “The gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.” People don’t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said.
“We don’t need to replicate all of the insulin-making function of beta cells,” he said. “Only 20 percent restoration of this capacity is sufficient for a cure of Type 1.”
Here's their patent on this. Methods and compositions for in vivo induction of pancreatic beta cell formation |
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Post by agedhippie on Oct 27, 2017 7:45:57 GMT -5
IMO this is a very flawed study. Allowing the afrezza arm to administer insulin as much as they need to post meals doesn't make sense. Of course you will see better "time in range" when that group is allowed to continually admin insulin. The injectable group only does it once prior to their meal so why not same restriction with afrezza group? Ok, I’ll give it a try,,, the reason the injectible group only “does it once” is because the current Injectible Mealtime Insulin options stay in your system longer than it takes to digest a meal, this makes stacking Insulin for better blood glucose extremely dangerous. The reason the Afrezza group takes follow up doses, is because they can !! I’m quite sure there are lots of times when a PWD would like to take a follow up dose of injected RAA because of a miscalculation, but the time stamp of the product doesn’t allow them to safely do it, You wouldn’t wind up with a better glucose reading if you stacked an injectible RAA, you’d most likely wind up in the hospital or dead 💀 if this was even remotely possible, PWD would’ve been doing it. Just to be clear. Stacking RAA insulin is not dangerous in itself, I do it every day as does almost every diabetic. What is dangerous is stacking insulin by not accounting for insulin onboard. Pumps automatically adjust for stacking to avoid this and glucose meters outside the US do the same. Stacking is no big deal. People don't do follow up doses because they can't be bothered and not because of fear of stacking. As a practical example I might eat at 8pm taking 8u of insulin. Three hours later I want to go to bed so I test and I find I am at 190 (Ok I admit it I had the dessert and didn't bolus). I need 3u to fix this but I still have 2u of insulin in my system (humalog lasts 4 hours with me) so I take 1u. I have just stacked insulin and all will be well. Now if I had not deducted the 2u I still had onboard I would stacked insulin and have woken up around 2am in a sweaty heap with a horrible low. Stacking insulin is something insulin users do routinely, even Afrezza insulin users (test 1 hour after the meal and take a second dose if required - Afrezza lasts two hours so they just stacked) That was a lot longer than I intended but I hope it explains stacking. |
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Post by akemp3000 on Oct 27, 2017 8:41:27 GMT -5
Here's another simple explanation: A healthy pancreas provides insulin whenever needed. With diabetics, Afrezza can also provide the necessary human insulin whenever needed. This gives diabetics a near normal improved quality of life. At such time following meals, when additional insulin is no longer needed, Afrezza leaves the body more rapidly than any other option. This is especially important at night as it greatly reduces the chance of hypoglycemia that too often can result in hospitalization or death. The simple explanation is that RAA's cannot do this.
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Tinkerbell
Researcher
Watcher of the Skies
Posts: 143
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Post by Tinkerbell on Oct 27, 2017 8:57:04 GMT -5
Let's be clear regarding the use of injectable insulin.
It doesn't matter if I'm on a study or not - if I, as a diabetic subject under study feel I need another does of injected insulin to control my blood sugar, I will take it. It will be recorded by the CGM and it will be recorded by me. In the end, the CGM will provided all data to be examined. The number of injectable doses of insulin will not matter one bit.
The protocol states that the 30 who remain on their usual insulin are to treat themselves as they usually do. Maybe there will be a few who take a second dose of injected - who knows. Even if they do, the data will tell us so and we will still analyze the endpoints as stated in the protocol. Safety first.
There is no argument here about any additional injectable insulins being problematic. It does not disqualify the subject if they decide they need to take another dose of injectable insulin. The statistical section of the protocol will set that straight. Got it?
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Post by babaoriley on Oct 27, 2017 9:01:04 GMT -5
Dr. DeFronzo could be pushing his message about the dangers of taking insulin because he is a co-inventor of a new gene transfer therapy that causes other cells to produce insulin in response to glucose, which would replace damaged, non-insulin producing pancreatic beta cells of patients with Type 1 diabetes.
Source: news.uthscsa.edu/diabetes-breakthrough-increases-insulin-producing-cells/
Excerpts:
A potential cure for Type 1 diabetes looms on the horizon in San Antonio, and the novel approach would also allow Type 2 diabetics to stop insulin shots.
The discovery, made at UT Health San Antonio, increases the types of pancreatic cells that secrete insulin. Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes at UT Health, is co-inventor on the patent. He described the therapy:
“The pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],” he said. “This is basically just like beta cells.”
Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn’t use insulin efficiently.
The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin. Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body’s immune defenses.
“If a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” Dr. DeFronzo said.
The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored. “A major problem we have in the field of Type 1 diabetes is hypoglycemia (low blood sugar),” Dr. Doiron said. “The gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.” People don’t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said.
“We don’t need to replicate all of the insulin-making function of beta cells,” he said. “Only 20 percent restoration of this capacity is sufficient for a cure of Type 1.”
That's fantastic news for mice! |
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Post by dreamboatcruise on Oct 27, 2017 11:44:07 GMT -5
babaoriley... they must have better health plans than people. All the cures seem to come for mice first. Often they don't ever make it to the human population.
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Post by mnholdem on Oct 27, 2017 11:51:51 GMT -5
So this will mean that mice won't have to carry around insulin syringes anymore? Excellent!
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Post by straightly on Oct 27, 2017 15:01:47 GMT -5
So this will mean that mice won't have to carry around insulin syringes anymore? Excellent! So they can change some cells to produce some insuline. Sounds like a heavenly match for Afrezza. When one eats and these cells cannot produce enough, Afrezza will take edge/spike off. Here is the hope for the diabetes lifes getting better. |
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Post by sayhey24 on Oct 27, 2017 15:55:41 GMT -5
Let's be clear regarding the use of injectable insulin. It doesn't matter if I'm on a study or not - if I, as a diabetic subject under study feel I need another does of injected insulin to control my blood sugar, I will take it. It will be recorded by the CGM and it will be recorded by me. In the end, the CGM will provided all data to be examined. The number of injectable doses of insulin will not matter one bit. The protocol states that the 30 who remain on their usual insulin are to treat themselves as they usually do. Maybe there will be a few who take a second dose of injected - who knows. Even if they do, the data will tell us so and we will still analyze the endpoints as stated in the protocol. Safety first. There is no argument here about any additional injectable insulins being problematic. It does not disqualify the subject if they decide they need to take another dose of injectable insulin. The statistical section of the protocol will set that straight. Got it? Thanks for reading the study protocol. This makes sense. |
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