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Post by sayhey24 on Jun 6, 2022 18:57:46 GMT -5
"the International Diabetes Center, described the center’s new approach to basal insulin therapy, called “CGM Clinician Guided Management,” to help healthcare providers recommend insulin adjustments using a person’s AGP report. Specifically, the provider would make a recommendation based on whether someone has diabetes-related complications that warrant the use of a GLP-1 receptor agonist or an SGLT-2 inhibitor, and their Time in Range (TIR) and Time Below Range (TBR) percentages" diatribe.org/using-insulin-type-2-diabetes-leveraging-technologyI think Mike needs to call Dr. Thomas Martens and introduce him to afrezza and demonstrate how afrezza should be used before a basal to address the issue all T2s face early in their diagnosis and that is loss of PPG control. Who knows, maybe the International Diabetes Center will want to publish their own standard of care. |
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Post by Deleted on Jun 6, 2022 20:15:37 GMT -5
That sounds too much like right....
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Post by sayhey24 on Jun 7, 2022 4:56:35 GMT -5
I just find it amazing that after having CGMs widely available for about 10 years the medical community still does not seem to understand that the first thing the T2s lose is post prandial glucose control. At least now we have the diet tech companies starting to understand that their diet clients are losing PPG control prior to weight gain but we still have the medical community wanting to address meal time control with a fasting insulin.
Its kind of mind blowing. It reminds me of the guy who thought he could fix everything with a hammer. Got a nail, I have a hammer. Got a screw, I have a hammer. My goodness, when basal insulin does not address PPG control, lets add a GLP1! What are these guys thinking? We do have the proper tools and it would sure be nice if someone started using them.
I see Bud Harris thought things were "Buzzing" at ADA2022. Working with the International Diabetes Center might be a good marketing opportunity for "Buzz" to move the ball down field.
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Post by agedhippie on Jun 9, 2022 14:43:44 GMT -5
I just find it amazing that after having CGMs widely available for about 10 years the medical community still does not seem to understand that the first thing the T2s lose is post prandial glucose control. At least now we have the diet tech companies starting to understand that their diet clients are losing PPG control prior to weight gain but we still have the medical community wanting to address meal time control with a fasting insulin. Its kind of mind blowing. It reminds me of the guy who thought he could fix everything with a hammer. Got a nail, I have a hammer. Got a screw, I have a hammer. My goodness, when basal insulin does not address PPG control, lets add a GLP1! What are these guys thinking? We do have the proper tools and it would sure be nice if someone started using them. I see Bud Harris thought things were "Buzzing" at ADA2022. Working with the International Diabetes Center might be a good marketing opportunity for "Buzz" to move the ball down field. That post prandial control goes first has been known for a long time (decades) which is why you have the OGTT, Oral Glucose tolerance test, as part of the diagnosis for Type 2. Type 2 is mostly a disease of relative insulin deficiency (insulin resistance means I don't have enough) rather than Type 1 which is an absolute deficiency (I don't have insulin at all!) Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output. This also addresses the problem of over production of glucagon by their alpha cells causing their liver to dump more glucose than it should into their blood since the basal insulin can cover that as well. Smart use of your own insulin is important because it is the best integrated, fastest act, most accurate dosing, and quickest clearing insulin there is so don't waste it on dumb basal glucose loads. To the hammer analogy - it is also true for insulin. Type 2 diabetes is a complex metabolic disorder of which high blood sugar is just the most visible symptom. Insulin treats that particular symptom, but does not address the other issues of diabetes. Endos know this which is why an insulin only approach is not credible for them, although I do wish they would add insulin sooner. |
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Post by buyitonsale on Jun 9, 2022 16:43:43 GMT -5
I feel sorry for all T2D patients that see a doctor for help and do not get the correct information from their doctor regarding the root cause for their "disease" and the fact that instead of running their health, these patients are actually in control to reverse this condition and rebuild their health. Shame on the doctors that are either clueless or do not care to explain it to the patients.
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Post by sayhey24 on Jun 9, 2022 17:22:10 GMT -5
I just find it amazing that after having CGMs widely available for about 10 years the medical community still does not seem to understand that the first thing the T2s lose is post prandial glucose control. At least now we have the diet tech companies starting to understand that their diet clients are losing PPG control prior to weight gain but we still have the medical community wanting to address meal time control with a fasting insulin. Its kind of mind blowing. It reminds me of the guy who thought he could fix everything with a hammer. Got a nail, I have a hammer. Got a screw, I have a hammer. My goodness, when basal insulin does not address PPG control, lets add a GLP1! What are these guys thinking? We do have the proper tools and it would sure be nice if someone started using them. I see Bud Harris thought things were "Buzzing" at ADA2022. Working with the International Diabetes Center might be a good marketing opportunity for "Buzz" to move the ball down field. That post prandial control goes first has been known for a long time (decades) which is why you have the OGTT, Oral Glucose tolerance test, as part of the diagnosis for Type 2. Type 2 is mostly a disease of relative insulin deficiency (insulin resistance means I don't have enough) rather than Type 1 which is an absolute deficiency (I don't have insulin at all!) Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output. This also addresses the problem of over production of glucagon by their alpha cells causing their liver to dump more glucose than it should into their blood since the basal insulin can cover that as well. Smart use of your own insulin is important because it is the best integrated, fastest act, most accurate dosing, and quickest clearing insulin there is so don't waste it on dumb basal glucose loads. To the hammer analogy - it is also true for insulin. Type 2 diabetes is a complex metabolic disorder of which high blood sugar is just the most visible symptom. Insulin treats that particular symptom, but does not address the other issues of diabetes. Endos know this which is why an insulin only approach is not credible for them, although I do wish they would add insulin sooner. Aged - you said "Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output" Thats not how the body works. During meal time the body needs a big dump of insulin not a little stream. The first thing the T2 loses is first phase insulin release which is a big dump. The basal is not replacing that. The basal will help to provide some stress relief on the beta cells but its a far cry from taking a big puff of afrezza and stopping the post meal spike. With the basal you will still see that post meal spike on your CGM and it will take a long time to come down. With afrezza, boom the PWD gets back to baseline just like a non-diabetic. Don't get me wrong. Taking the basal is better than taking the orals but it is not even close to taking afrezza at meal time. You said "Smart use of your own insulin is important because it is the best integrated" Yes, that is why you want to take the afrezza at meal time, stop the spike, get the PWD back to baseline and take the load off the pancreas so it can cover the fasting period and hopefully the reduced stress will allow beta cell regeneration. The more you can take that post meal stress off the beta cells the better chance at stopping and maybe even reversing progression. |
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Post by agedhippie on Jun 9, 2022 18:24:57 GMT -5
Aged - you said "Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output" Thats not how the body works. During meal time the body needs a big dump of insulin not a little stream. The first thing the T2 loses is first phase insulin release which is a big dump. The basal is not replacing that. The basal will help to provide some stress relief on the beta cells but its a far cry from taking a big puff of afrezza and stopping the post meal spike. With the basal you will still see that post meal spike on your CGM and it will take a long time to come down. With afrezza, boom the PWD gets back to baseline just like a non-diabetic. Don't get me wrong. Taking the basal is better than taking the orals but it is not even close to taking afrezza at meal time. You said "Smart use of your own insulin is important because it is the best integrated" Yes, that is why you want to take the afrezza at meal time, stop the spike, get the PWD back to baseline and take the load off the pancreas so it can cover the fasting period and hopefully the reduced stress will allow beta cell regeneration. The more you can take that post meal stress off the beta cells the better chance at stopping and maybe even reversing progression. Sorry, but that's exactly how the body works. You lose first phase because you are spending insulin on basal so your beta cells are already depleted when the food arrives so all you have is second phase. If you are not doing that then the beta cells are not stressed and can deliver. This is exactly why you use basal insulin in Type 2. Now insulin resistance will continue to build because you have a broken metabolism and there will come a point where basal alone cannot make up the deficit. I have yet to see a trial that proves this does not happen with Afrezza over the long haul and I would be surprised if it didn't because that metabolism is continuing it's slow motion trainwreck in the background. Afrezza is only loosely comparable to your own insulin. The underlying mechanisms and controls are as different as chalk and cheese, the only similarity is the chemical composition. All the supporting interactions are missing. I do agree that removing the demand from the beta cells will help for a while. |
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Post by georgethenight2 on Jun 10, 2022 4:04:26 GMT -5
Aged - you said "Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output" Thats not how the body works. During meal time the body needs a big dump of insulin not a little stream. The first thing the T2 loses is first phase insulin release which is a big dump. The basal is not replacing that. The basal will help to provide some stress relief on the beta cells but its a far cry from taking a big puff of afrezza and stopping the post meal spike. With the basal you will still see that post meal spike on your CGM and it will take a long time to come down. With afrezza, boom the PWD gets back to baseline just like a non-diabetic. Don't get me wrong. Taking the basal is better than taking the orals but it is not even close to taking afrezza at meal time. You said "Smart use of your own insulin is important because it is the best integrated" Yes, that is why you want to take the afrezza at meal time, stop the spike, get the PWD back to baseline and take the load off the pancreas so it can cover the fasting period and hopefully the reduced stress will allow beta cell regeneration. The more you can take that post meal stress off the beta cells the better chance at stopping and maybe even reversing progression. Sorry, but that's exactly how the body works. You lose first phase because you are spending insulin on basal so your beta cells are already depleted when the food arrives so all you have is second phase. If you are not doing that then the beta cells are not stressed and can deliver. This is exactly why you use basal insulin in Type 2. Now insulin resistance will continue to build because you have a broken metabolism and there will come a point where basal alone cannot make up the deficit. I have yet to see a trial that proves this does not happen with Afrezza over the long haul and I would be surprised if it didn't because that metabolism is continuing it's slow motion trainwreck in the background. Afrezza is only loosely comparable to your own insulin. The underlying mechanisms and controls are as different as chalk and cheese, the only similarity is the chemical composition. All the supporting interactions are missing. I do agree that removing the demand from the beta cells will help for a while. Still here after so many years of being a non investor. I really appreciate others and their opinions. But, aged. Second drug FDA approved bro. Don't you have some foot fungus to attend to. Better yet, what don't tell us how LQDA is going to prevail over United and its hoards of cash and experience. So glad to be here, but time for the skeptics to be silenced. No black box. No electrical outlets necessary. Expanding patient population. Do I need to go on. As for Afrezza. It's now only a waiting game. Your patent ending drug, our patent expanding tech and know how. I would say something rude, but FDA approved should be just fine. Just puff Aged, it's the cool thing man! |
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Post by sayhey24 on Jun 10, 2022 7:11:33 GMT -5
Aged - you said "Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output" Thats not how the body works. During meal time the body needs a big dump of insulin not a little stream. The first thing the T2 loses is first phase insulin release which is a big dump. The basal is not replacing that. The basal will help to provide some stress relief on the beta cells but its a far cry from taking a big puff of afrezza and stopping the post meal spike. With the basal you will still see that post meal spike on your CGM and it will take a long time to come down. With afrezza, boom the PWD gets back to baseline just like a non-diabetic. Don't get me wrong. Taking the basal is better than taking the orals but it is not even close to taking afrezza at meal time. You said "Smart use of your own insulin is important because it is the best integrated" Yes, that is why you want to take the afrezza at meal time, stop the spike, get the PWD back to baseline and take the load off the pancreas so it can cover the fasting period and hopefully the reduced stress will allow beta cell regeneration. The more you can take that post meal stress off the beta cells the better chance at stopping and maybe even reversing progression. Sorry, but that's exactly how the body works. You lose first phase because you are spending insulin on basal so your beta cells are already depleted when the food arrives so all you have is second phase. If you are not doing that then the beta cells are not stressed and can deliver. This is exactly why you use basal insulin in Type 2. Now insulin resistance will continue to build because you have a broken metabolism and there will come a point where basal alone cannot make up the deficit. I have yet to see a trial that proves this does not happen with Afrezza over the long haul and I would be surprised if it didn't because that metabolism is continuing it's slow motion trainwreck in the background. Afrezza is only loosely comparable to your own insulin. The underlying mechanisms and controls are as different as chalk and cheese, the only similarity is the chemical composition. All the supporting interactions are missing. I do agree that removing the demand from the beta cells will help for a while. Aged - now you are going to get Mango upset. Afrezza is not loosely comparable to your own insulin. Afrezza is human insulin. Its not an RAA or some other GLP1 type thing. At the molecular level it is identical to what the human body makes. Yes, this is not true for the RAA but it is for afrezza. Mango can go into the details on how its the only insulin to work hand in hand with the liver just like you were non-diabetic. Now - you lose first phase release because you are losing beta cell mass and you don't have enough beta cells to catch up after eating and store the needed insulin for first phase release. We know from autopsy that there is reduce beta cell mass in PWDs. (If we believe Joslin's research then some of insulin stored is also bad) Between trying to pump out insulin to bring down the post meal spike and the additional stress of pumping out insulin for fasting needs the pancreas is working overtime and can't recover. Think of it like running a marathon on a sprained ankle. If you keeping runnning on it it will get worse and worse over time and there is a pretty good chance by the end of the 26 miles you may not be able to walk. That is the pancreas of the T2 over time. Ask that runner to sprint after the race is not happening and thats first phase release. Put that runner in a wheelchair and rest the foot and there is a pretty good chance their ankle will recover. |
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Post by agedhippie on Jun 10, 2022 8:00:16 GMT -5
Still here after so many years of being a non investor. I really appreciate others and their opinions. But, aged. Second drug FDA approved bro. Don't you have some foot fungus to attend to. Better yet, what don't tell us how LQDA is going to prevail over United and its hoards of cash and experience. So glad to be here, but time for the skeptics to be silenced. No black box. No electrical outlets necessary. Expanding patient population. Do I need to go on. As for Afrezza. It's now only a waiting game. Your patent ending drug, our patent expanding tech and know how. I would say something rude, but FDA approved should be just fine. Just puff Aged, it's the cool thing man! Why do you think I like LQDA? You seem confused. |
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Post by georgethenight2 on Jun 10, 2022 8:03:36 GMT -5
Still here after so many years of being a non investor. I really appreciate others and their opinions. But, aged. Second drug FDA approved bro. Don't you have some foot fungus to attend to. Better yet, what don't tell us how LQDA is going to prevail over United and its hoards of cash and experience. So glad to be here, but time for the skeptics to be silenced. No black box. No electrical outlets necessary. Expanding patient population. Do I need to go on. As for Afrezza. It's now only a waiting game. Your patent ending drug, our patent expanding tech and know how. I would say something rude, but FDA approved should be just fine. Just puff Aged, it's the cool thing man! Why do you think I like LQDA? You seem confused. Are you long MNKD? |
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Post by agedhippie on Jun 10, 2022 8:06:11 GMT -5
Why do you think I like LQDA? You seem confused. Are you long MNKD? I was pre-split. Still waiting for it to get back to the split price where I feel it would be safe to get back in. I did do quite nicely with options on the FDA clearance though  |
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Post by agedhippie on Jun 10, 2022 8:31:22 GMT -5
Aged - now you are going to get Mango upset. Afrezza is not loosely comparable to your own insulin. Afrezza is human insulin. Its not an RAA or some other GLP1 type thing. At the molecular level it is identical to what the human body makes. Yes, this is not true for the RAA but it is for afrezza. Mango can go into the details on how its the only insulin to work hand in hand with the liver just like you were non-diabetic. I phrased that badly. The molecule is the same, but the delivery mechanism is completely different. The body will release insulin in expectation of food as well as in response to food, it will release what is needed rather than one of three size doses, and it will continuously modify the level of insulin in the blood. The net result is that it is faster in and faster out while also being able to respond to late arriving spikes and feed back from muscles and duodenum as well as the liver. Afrezza is a raw dollop of insulin dumped into the blood stream while no modulation or follow up - same issue as RAA. Afrezza is better than RAA because of the faster absorption and clearance. RAA needs to make it's way in from subq so it arrives in dribs and drabs which makes clearance harder, while Afrezza arrives all in one dollop, but you don't get that tail so clearance is faster. There are papers on the plasticity of beta cells. The conclusion is that initially beta cells shut down, and then eventually die. You can restore first phase if you relieve the stress during that period. After that phase the cells start to die and your safety margin begins to disappear until the point where you can no longer recover. A good example of this shut down, although rather more severe than in regular Type 2, is the Flatbush Type 2 variant where the beta cells abruptly and completely shut down but after about six weeks on insulin restart (it's an odd variant as that shutdown may only happen once or twice in your life). I think that was a long winded way of saying I agree that removing oxidative stress will give shut down but not dead beta cells the chance to recover, and not removing it will kill them. You see this in the honeymoon phase with Type 1 where after an initial collapse and treatment you can go for months with minimal insulin needs as you bring the overstressed beta cells back on-line (eventually your immune system eats them though  ) |
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Post by mango on Jun 10, 2022 9:29:48 GMT -5
I just find it amazing that after having CGMs widely available for about 10 years the medical community still does not seem to understand that the first thing the T2s lose is post prandial glucose control. At least now we have the diet tech companies starting to understand that their diet clients are losing PPG control prior to weight gain but we still have the medical community wanting to address meal time control with a fasting insulin. Its kind of mind blowing. It reminds me of the guy who thought he could fix everything with a hammer. Got a nail, I have a hammer. Got a screw, I have a hammer. My goodness, when basal insulin does not address PPG control, lets add a GLP1! What are these guys thinking? We do have the proper tools and it would sure be nice if someone started using them. I see Bud Harris thought things were "Buzzing" at ADA2022. Working with the International Diabetes Center might be a good marketing opportunity for "Buzz" to move the ball down field. That post prandial control goes first has been known for a long time (decades) which is why you have the OGTT, Oral Glucose tolerance test, as part of the diagnosis for Type 2. Type 2 is mostly a disease of relative insulin deficiency (insulin resistance means I don't have enough) rather than Type 1 which is an absolute deficiency (I don't have insulin at all!) Giving Type 2 diabetics basal insulin allows them to use their own insulin for meals rather than waste it on their basal glucose output. This also addresses the problem of over production of glucagon by their alpha cells causing their liver to dump more glucose than it should into their blood since the basal insulin can cover that as well. Smart use of your own insulin is important because it is the best integrated, fastest act, most accurate dosing, and quickest clearing insulin there is so don't waste it on dumb basal glucose loads. To the hammer analogy - it is also true for insulin. Type 2 diabetes is a complex metabolic disorder of which high blood sugar is just the most visible symptom. Insulin treats that particular symptom, but does not address the other issues of diabetes. Endos know this which is why an insulin only approach is not credible for them, although I do wish they would add insulin sooner. Aged, it’s medically incorrect to put a T2D on basal insulin. T2Ds have a diminished, ineffective first phase response, also known as an eating-induced insulin secretion response. All the “other problems” are because of dysregulation of post prandial glucose homeostasis. Afrezza fixes this. In fact, it’s the only insulin currently on the market that is capable of fixing the underlying defect in T2D which is the loss of the eating-induced insulin response. Afrezza mimics physiologic prandial insulin secretion. No other mealtime insulin has the pharmacokinetics to achieve this. Sayhey is correct. It’s absolutely absurd we put T2Ds on basal and all these orals which do not address the underlying issue which is a diminished or loss of eating-induced insulin secretion (PFIR), and thus, dysregulated post prandial glucose homeostasis. You’re incorrect about Afrezza. It is identical to endogenous human insulin, and matches physiologic eating-induced insulin secretion like that seen in a healthy, non diabetic human. There’s no difference with Afrezza and what is seen in a non-diabetic. This is why and how it restores post prandial glucose homeostasis, effectively replacing the eating-induced insulin secretion that was ineffective and led to dysregulation of post prandial glucose homeostasis. |
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Post by agedhippie on Jun 10, 2022 10:55:00 GMT -5
Aged, it’s medically incorrect to put a T2D on basal insulin. T2Ds have a diminished, ineffective first phase response, also known as an eating-induced insulin secretion response. All the “other problems” are because of dysregulation of post prandial glucose homeostasis. Afrezza fixes this. In fact, it’s the only insulin currently on the market that is capable of fixing the underlying defect in T2D which is the loss of the eating-induced insulin response. Afrezza mimics physiologic prandial insulin secretion. No other mealtime insulin has the pharmacokinetics to achieve this. This where we differ. You seem to see Type 2 as a result of and insulin deficiency and all the associated issues like high BP, lipid disfunction, insulin resistance, alpha cell disfunction, etc. as a result of that. The medical world sees those as a broken metabolism usually referred to as Metabolic Syndrome. I am in that latter camp, I think hyperglycemia is just one aspect of Metabolic Syndrome. Sorting out post prandial meal spikes does not fix all the other issues and those continue to drive hyperglycemia (alpha cells, excessive basal output, increasing insulin resistance in muscles). You can restore glucose homostasis for a while via diet and/or weight loss since both reduce the demand on the pancreas and allow you to live within your insulin budget. Depending on how aggressive the Metabolic Syndrome is (which genes are involved) that can result in almost indefinite remission, or buy you a few years. |
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