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Post by sayhey24 on Jun 10, 2017 8:05:23 GMT -5
Based on one article about the Apple Watch CGM effort it appears that Apple is taking the approach of not officially targeting it for use by patients with diabetes... it is officially meant for use by the general population. Supposedly to get around need for FDA approval. That is double edge sword, however. Obviously big benefit in time to market, but insurance isn't going to pay for a device that isn't FDA approved. I would assume many PWD might choose to buy one anyway, especially if they already use an iPhone... if I had diabetes I'd likely want a non-invasive CGM even if not as accurate as finger stick... though unlikely to switch to Apple from Android just to get CGM with Apple Watch. I would be very resistant to using an invasive CGM, myself. quote: Apple is taking the approach of not officially targeting it for use by patients with diabetes... it is officially meant for use by the general population. Supposedly to get around need for FDA approval. reply: brilliant. We know how many people own iphones. people with iphones will enjoy the application. I will buy a new iphone just for the application. it really is fun to see what blood, Interstitial glucose does with food and exercise.
Peppy - the Apple won't be available for awhile. I wish it was today. Hopefully Mike got Dachis to get some prototypes and some MNKD people are wearing them at ADA 77. In the meantime for kicks- Download this app www.librelink.com/ for your android. Set your country code to the UK or Germany if you are in the U.S. Go on ebay and buy some sensors for $70-80 per sensor. You can then send the data on your phone to Dachis's software. |
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Post by peppy on Jun 10, 2017 8:22:22 GMT -5
When I explain the value of the A1c measurement to people I equate it to a car's "average miles per gallon". A1c is really not much use when on a day to day, hour to hour basis a PWD needs to know what their current sugar level is. What they need is a speedometer which we now have with continuous glucose monitors. Now an A1c of 5.7 is about an average BG level of 111. The question which needs to be asked is what is the PWD's BG 1hour and 2 hours after eating and eating what as only carbs will raise sugar levels. Most T2s currently being treated with metformin are seeing post meal spikes over 200+. They then spend hours over 140 which is considered the magic number for microvasclular damage. Metformin does nothing to address root cause - not enough insulin at meal time. The SGLT2 and other non-insulin treatments just create a bigger mess. The real question is does the medical community want to address the root cause of T2 diabetes which is the pancreas not producing enough insulin at meal time or not? I am not so sure. Maybe if they understood diabetes better and the current medications better some would. There is only one way to address meal time sugar spikes and that is mealtime insulin. CGMs make things so easy and the introduction of the Abbott Libre which Mike C said should be available in the U.S. soon make CGMs almost affordable for everyone. I suspect many doctors want to continue to treat T2 diabetes as a black art and keep the PWDs in the dark. There is an ADA session Sunday at 2pm as to whether T2's should be using CGMs. Thats almost like asking should cars have speedometers. I am hoping Dachis is showing at ADA with the Libre interfacing with an android and then sending that data to his monitoring system. The NFC andriod app is already available from Abbott. I also see David Cheng is back at ADA with Glutalor which is the San Meditec CGM from China. This is a CGM which could be brought to markets for pennies on the dollar compared to the Dexcom and its #1 in China. quote: The real question is does the medical community want to address the root cause of T2 diabetes which is the pancreas not producing enough insulin at meal time or not? I am not so sure. reply: It looks to me like the medical community wants to prescribe the status quo drugs.
Quote: Maybe if they understood diabetes better and the current medications better some would reply: I thought the physicians whole job was to understand the medications they prescribe.
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Post by agedhippie on Jun 10, 2017 9:17:24 GMT -5
Based on one article about the Apple Watch CGM effort it appears that Apple is taking the approach of not officially targeting it for use by patients with diabetes... it is officially meant for use by the general population. Supposedly to get around need for FDA approval. That is double edge sword, however. Obviously big benefit in time to market, but insurance isn't going to pay for a device that isn't FDA approved. I would assume many PWD might choose to buy one anyway, especially if they already use an iPhone... if I had diabetes I'd likely want a non-invasive CGM even if not as accurate as finger stick... though unlikely to switch to Apple from Android just to get CGM with Apple Watch. I would be very resistant to using an invasive CGM, myself. The Apple Watch app was introduced at the Apple's WWDC ( link here). Turns out it is the Dexcom Apple watch app and not some new Apple technology. Them see to be more interested in using low power Bluetooth (BLE) to have the iPhone aggregate data from several medical devices. Since the Dexcom G5 transmitter talks Bluetooth it's an obvious candidate and why Tim Cook was trying it out. It's a cool looking app. The non-invasive CGMs are still a long way off in my opinion. The problem is that the optical approach is affected by things like dehydration and selection (glucose doesn't absorb IR light well so you get false readings). Really you need access to body fluids which is why Google used that contact lens. |
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Post by peppy on Jun 10, 2017 9:30:56 GMT -5
Based on one article about the Apple Watch CGM effort it appears that Apple is taking the approach of not officially targeting it for use by patients with diabetes... it is officially meant for use by the general population. Supposedly to get around need for FDA approval. That is double edge sword, however. Obviously big benefit in time to market, but insurance isn't going to pay for a device that isn't FDA approved. I would assume many PWD might choose to buy one anyway, especially if they already use an iPhone... if I had diabetes I'd likely want a non-invasive CGM even if not as accurate as finger stick... though unlikely to switch to Apple from Android just to get CGM with Apple Watch. I would be very resistant to using an invasive CGM, myself. The Apple Watch app was introduced at the Apple's WWDC ( link here). Turns out it is the Dexcom Apple watch app and not some new Apple technology. Them see to be more interested in using low power Bluetooth (BLE) to have the iPhone aggregate data from several medical devices. Since the Dexcom G5 transmitter talks Bluetooth it's an obvious candidate and why Tim Cook was trying it out. It's a cool looking app. The non-invasive CGMs are still a long way off in my opinion. The problem is that the optical approach is affected by things like dehydration and selection (glucose doesn't absorb IR light well so you get false readings). Really you need access to body fluids which is why Google used that contact lens. my pea brain has a difficult time understanding why pulse oximeters can determine the O2 saturation of hemoglobin, the device working on a finger or toe (so capillary), while a device can not be enabled to read the glucose in the blood stream/interstitial fluid. Have any incite aged/all?
gluco-wise.com/beta/ How does GlucoWise™ measure my blood glucose levels without taking any blood?The glucose levels are extracted by a non-invasive technique which transmits low-power radio waves through a section of the human body, such as the area between the thumb and forefinger or the earlobe. These areas have adequate blood concentration and are thin enough for waves to pass through the tissue. These signals are then received by a sensor on the opposite side, where the data about the properties of the blood within the flesh are collected and analyzed.
So I have heard this stuff all my life. It can't be done. free-energy.ws/nikola-tesla/
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Post by agedhippie on Jun 10, 2017 9:49:47 GMT -5
The Apple Watch app was introduced at the Apple's WWDC ( link here). Turns out it is the Dexcom Apple watch app and not some new Apple technology. Them see to be more interested in using low power Bluetooth (BLE) to have the iPhone aggregate data from several medical devices. Since the Dexcom G5 transmitter talks Bluetooth it's an obvious candidate and why Tim Cook was trying it out. It's a cool looking app. The non-invasive CGMs are still a long way off in my opinion. The problem is that the optical approach is affected by things like dehydration and selection (glucose doesn't absorb IR light well so you get false readings). Really you need access to body fluids which is why Google used that contact lens. my pea brain has a difficult time understanding why pulse oximeters can determine the O2 saturation of hemoglobin, the device working on a finger or toe (so capillary), while a device can not be enabled to read the glucose in the blood stream/interstitial fluid. Have any incite aged/all?
gluco-wise.com/beta/
So I have heard this stuff all my life. It can't be done. free-energy.ws/nikola-tesla/
Hemoglobin absorbs light at certain frequencies really well and glucose doesn't. Worse, hemoglobin blocks the light you need to measure the glucose! To get a good reading you need to go into the far infrared but then you get extremely shallow penetration and cannot see the blood. The Japanese are working on a far IR sensor that reads the inside of the mouth because blood vessels are closest to the surface there. The Gluco-Wise solution interests me because they use microwaves rather than light to take the reading. I will have to look further into that. Thank you for the Tesla link. That was fascinating. |
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Post by peppy on Jun 10, 2017 10:23:10 GMT -5
my pea brain has a difficult time understanding why pulse oximeters can determine the O2 saturation of hemoglobin, the device working on a finger or toe (so capillary), while a device can not be enabled to read the glucose in the blood stream/interstitial fluid. Have any incite aged/all?
gluco-wise.com/beta/
So I have heard this stuff all my life. It can't be done. free-energy.ws/nikola-tesla/
Hemoglobin absorbs light at certain frequencies really well and glucose doesn't. Worse, hemoglobin blocks the light you need to measure the glucose! To get a good reading you need to go into the far infrared but then you get extremely shallow penetration and cannot see the blood. The Japanese are working on a far IR sensor that reads the inside of the mouth because blood vessels are closest to the surface there. The Gluco-Wise solution interests me because they use microwaves rather than light to take the reading. I will have to look further into that. Thank you for the Tesla link. That was fascinating. Thank you aged. The distinction microwaves aye? All our cell phones work on microwave frequencies. The iwatch, microwave length waves. hmmmm Aged, I love you.
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Post by nadathing on Jun 10, 2017 10:44:02 GMT -5
When I explain the value of the A1c measurement to people I equate it to a car's "average miles per gallon". A1c is really not much use when on a day to day, hour to hour basis a PWD needs to know what their current sugar level is. What they need is a speedometer which we now have with continuous glucose monitors. Now an A1c of 5.7 is about an average BG level of 111. The question which needs to be asked is what is the PWD's BG 1hour and 2 hours after eating and eating what as only carbs will raise sugar levels. Most T2s currently being treated with metformin are seeing post meal spikes over 200+. They then spend hours over 140 which is considered the magic number for microvasclular damage. Metformin does nothing to address root cause - not enough insulin at meal time. The SGLT2 and other non-insulin treatments just create a bigger mess. The real question is does the medical community want to address the root cause of T2 diabetes which is the pancreas not producing enough insulin at meal time or not? I am not so sure. Maybe if they understood diabetes better and the current medications better some would. There is only one way to address meal time sugar spikes and that is mealtime insulin. CGMs make things so easy and the introduction of the Abbott Libre which Mike C said should be available in the U.S. soon make CGMs almost affordable for everyone. I suspect many doctors want to continue to treat T2 diabetes as a black art and keep the PWDs in the dark. There is an ADA session Sunday at 2pm as to whether T2's should be using CGMs. Thats almost like asking should cars have speedometers. I am hoping Dachis is showing at ADA with the Libre interfacing with an android and then sending that data to his monitoring system. The NFC andriod app is already available from Abbott. I also see David Cheng is back at ADA with Glutalor which is the San Meditec CGM from China. This is a CGM which could be brought to markets for pennies on the dollar compared to the Dexcom and its #1 in China. I've been T2 for almost 15 years. You seen to be quite knowledgeable on diabetes. Please correct me if I'm wrong. I was told by my doctor that diabetes may be one of these or a combination of all three or two: Pancreas not making insulin or insufficient insulin. Red blood cells are resistant to insulin. Liver produces too much glucose. Thanks. |
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Post by sayhey24 on Jun 10, 2017 12:05:34 GMT -5
When I explain the value of the A1c measurement to people I equate it to a car's "average miles per gallon". A1c is really not much use when on a day to day, hour to hour basis a PWD needs to know what their current sugar level is. What they need is a speedometer which we now have with continuous glucose monitors. Now an A1c of 5.7 is about an average BG level of 111. The question which needs to be asked is what is the PWD's BG 1hour and 2 hours after eating and eating what as only carbs will raise sugar levels. Most T2s currently being treated with metformin are seeing post meal spikes over 200+. They then spend hours over 140 which is considered the magic number for microvasclular damage. Metformin does nothing to address root cause - not enough insulin at meal time. The SGLT2 and other non-insulin treatments just create a bigger mess. The real question is does the medical community want to address the root cause of T2 diabetes which is the pancreas not producing enough insulin at meal time or not? I am not so sure. Maybe if they understood diabetes better and the current medications better some would. There is only one way to address meal time sugar spikes and that is mealtime insulin. CGMs make things so easy and the introduction of the Abbott Libre which Mike C said should be available in the U.S. soon make CGMs almost affordable for everyone. I suspect many doctors want to continue to treat T2 diabetes as a black art and keep the PWDs in the dark. There is an ADA session Sunday at 2pm as to whether T2's should be using CGMs. Thats almost like asking should cars have speedometers. I am hoping Dachis is showing at ADA with the Libre interfacing with an android and then sending that data to his monitoring system. The NFC andriod app is already available from Abbott. I also see David Cheng is back at ADA with Glutalor which is the San Meditec CGM from China. This is a CGM which could be brought to markets for pennies on the dollar compared to the Dexcom and its #1 in China. I've been T2 for almost 15 years. You seen to be quite knowledgeable on diabetes. Please correct me if I'm wrong. I was told by my doctor that diabetes may be one of these or a combination of all three or two: Pancreas not making insulin or insufficient insulin. Red blood cells are resistant to insulin. Liver produces too much glucose. Thanks. Your doctor is correct. The end result of any of the FOUR (insufficient and not making any are different) is you need more insulin. For T2s the time you really need the insulin is at meal time because this is when it spikes and you need to keep it under 140 or you risk microvascular disease. If your pancreas is still making insulin there is a good chance some or much of the beta cell function can be restored but you have to get your BG back to near normal (80 - 120) give or take for 3 to 6 months. What is your BG 1 hour and 2 hours after eating a low fat high carb meal? Most out of control T2s see it 200+, 300 is atypical. There are a zillion research papers on the reasons for insulin resistance but the end result for the most part is the chicken and egg discussion- did not enough insulin cause the resistance or did the resistance cause glucose toxicity which killed the beta cells. What is usually true is if you get your A1c into the 5s your insulin resistance will not be what it was AND you will most likely get some beta cell function back. We have 40+ years of research papers saying early insulin intervention results in a reversal of diabetes in T2s. Get it back to 5.0 and you are really in business. Also the more muscle mass you can build the more your resistance will lower. Afrezza, moderate carb and moderate-lower fat meal and some exercising - nice walk a couple miles a day- nothing crazy, will get most people in the 5's. Also when your BG spikes it seems the magic number is 180 where the body incurs temporary insulin resistance as a protective measure. Thats why if you watch some of the afrezza users in their youtubes they talk about needing more afrezza when they did not blunt the spike or forgot. Now, the problem for most T2s with the liver producing too much glucose is they have lost first phase insulin release at meal time and the liver is still dumping glucose into the blood. If you have normal phase one release this will shut off the liver. Diabetes is really an engineering flow control problem which Dr. Bernstein who was an engineer not a doctor at the time realized 30 years ago. Basically the liver, pancreas and other organs are out of sync because of high BG and its impacts. High sugars cause so many issues because its a funny thing about the blood, it just seems to be needed by the entire body. So to fix the liver issue you need to get your phase one insulin release back. There are currently only two ways to do this; a healthy pancreas; or a puff of afrezza. No other insulin or insulin analog not even the new Fiasp can provide this function which is critical. The liver needs that big robust hit. Metformin does limit insulin liver glucose production but not in a natural way and causes other issues. For example, 50% of metformin users are now developing Alzheimer's. The biggest thing is it does not address the root T2 issue - stopping the meal time BG spike. Hope this helps. |
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Post by centralcoastinvestor on Jun 10, 2017 13:03:57 GMT -5
I've been T2 for almost 15 years. You seen to be quite knowledgeable on diabetes. Please correct me if I'm wrong. I was told by my doctor that diabetes may be one of these or a combination of all three or two: Pancreas not making insulin or insufficient insulin. Red blood cells are resistant to insulin. Liver produces too much glucose. Thanks. Your doctor is correct. The end result of any of the FOUR (insufficient and not making any are different) is you need more insulin. For T2s the time you really need the insulin is at meal time because this is when it spikes and you need to keep it under 140 or you risk microvascular disease. If your pancreas is still making insulin there is a good chance some or much of the beta cell function can be restored but you have to get your BG back to near normal (80 - 120) give or take for 3 to 6 months. What is your BG 1 hour and 2 hours after eating a low fat high carb meal? Most out of control T2s see it 200+, 300 is atypical. There are a zillion research papers on the reasons for insulin resistance but the end result for the most part is the chicken and egg discussion- did not enough insulin cause the resistance or did the resistance cause glucose toxicity which killed the beta cells. What is usually true is if you get your A1c into the 5s your insulin resistance will not be what it was AND you will most likely get some beta cell function back. We have 40+ years of research papers saying early insulin intervention results in a reversal of diabetes in T2s. Get it back to 5.0 and you are really in business. Also the more muscle mass you can build the more your resistance will lower. Afrezza, moderate carb and moderate-lower fat meal and some exercising - nice walk a couple miles a day- nothing crazy, will get most people in the 5's. Also when your BG spikes it seems the magic number is 180 where the body incurs temporary insulin resistance as a protective measure. Thats why if you watch some of the afrezza users in their youtubes they talk about needing more afrezza when they did not blunt the spike or forgot. Now, the problem for most T2s with the liver producing too much glucose is they have lost first phase insulin release at meal time and the liver is still dumping glucose into the blood. If you have normal phase one release this will shut off the liver. Diabetes is really an engineering flow control problem which Dr. Bernstein who was an engineer not a doctor at the time realized 30 years ago. Basically the liver, pancreas and other organs are out of sync because of high BG and its impacts. High sugars cause so many issues because its a funny thing about the blood, it just seems to be needed by the entire body. So to fix the liver issue you need to get your phase one insulin release back. There are currently only two ways to do this; a healthy pancreas; or a puff of afrezza. No other insulin or insulin analog not even the new Fiasp can provide this function which is critical. The liver needs that big robust hit. Metformin does limit insulin liver glucose production but not in a natural way and causes other issues. For example, 50% of metformin users are now developing Alzheimer's. The biggest thing is it does not address the root T2 issue - stopping the meal time BG spike. Hope this helps. Great explanation. I'm always learning something from this board. Thanks for posting this. |
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Post by nadathing on Jun 10, 2017 14:16:25 GMT -5
I've been T2 for almost 15 years. You seen to be quite knowledgeable on diabetes. Please correct me if I'm wrong. I was told by my doctor that diabetes may be one of these or a combination of all three or two: Pancreas not making insulin or insufficient insulin. Red blood cells are resistant to insulin. Liver produces too much glucose. Thanks. Your doctor is correct. The end result of any of the FOUR (insufficient and not making any are different) is you need more insulin. For T2s the time you really need the insulin is at meal time because this is when it spikes and you need to keep it under 140 or you risk microvascular disease. If your pancreas is still making insulin there is a good chance some or much of the beta cell function can be restored but you have to get your BG back to near normal (80 - 120) give or take for 3 to 6 months. What is your BG 1 hour and 2 hours after eating a low fat high carb meal? Most out of control T2s see it 200+, 300 is atypical. There are a zillion research papers on the reasons for insulin resistance but the end result for the most part is the chicken and egg discussion- did not enough insulin cause the resistance or did the resistance cause glucose toxicity which killed the beta cells. What is usually true is if you get your A1c into the 5s your insulin resistance will not be what it was AND you will most likely get some beta cell function back. We have 40+ years of research papers saying early insulin intervention results in a reversal of diabetes in T2s. Get it back to 5.0 and you are really in business. Also the more muscle mass you can build the more your resistance will lower. Afrezza, moderate carb and moderate-lower fat meal and some exercising - nice walk a couple miles a day- nothing crazy, will get most people in the 5's. Also when your BG spikes it seems the magic number is 180 where the body incurs temporary insulin resistance as a protective measure. Thats why if you watch some of the afrezza users in their youtubes they talk about needing more afrezza when they did not blunt the spike or forgot. Now, the problem for most T2s with the liver producing too much glucose is they have lost first phase insulin release at meal time and the liver is still dumping glucose into the blood. If you have normal phase one release this will shut off the liver. Diabetes is really an engineering flow control problem which Dr. Bernstein who was an engineer not a doctor at the time realized 30 years ago. Basically the liver, pancreas and other organs are out of sync because of high BG and its impacts. High sugars cause so many issues because its a funny thing about the blood, it just seems to be needed by the entire body. So to fix the liver issue you need to get your phase one insulin release back. There are currently only two ways to do this; a healthy pancreas; or a puff of afrezza. No other insulin or insulin analog not even the new Fiasp can provide this function which is critical. The liver needs that big robust hit. Metformin does limit insulin liver glucose production but not in a natural way and causes other issues. For example, 50% of metformin users are now developing Alzheimer's. The biggest thing is it does not address the root T2 issue - stopping the meal time BG spike. Hope this helps. Thank you for your reply. This is one of the reasons I enjoy reading this board. I try to restrict my carb intake to 60 grams per meal. I try to stay compliant 80% of the time. I admit that I do not check my BG after I indulge in a large bowl of ice cream or eat more pizza than I should. I have no doubt it would be between 200 - 300. I take Metformin like most T2's. I take once weekly Trulicity since my insurance no longer covers Bydureon. A side affect of a GLP-1 is that it suppresses appetite. I do a lot of walking and dropped 41# over the years. My A1c stays between 5.6 - 5.8 and I have it checked twice a year. I was told that almost all T2's will become insulin dependent if they live long enough. Do you think Afrezza is appropriate for T2's who are not insulin dependent? My doctor (Internal Medicine) says no. Then again, she said that knowing it is insulin but has not been educated on the drug. Even more amazing is that this clinic is part of the same system that includes The International Diabetes Center in Minneapolis and is in the same building. I was told that her department does not see pharma reps. Pretty hard to get doctors on board when they aren't exposed to what is new on the market. |
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Post by mnholdem on Jun 10, 2017 14:22:35 GMT -5
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Post by peppy on Jun 10, 2017 15:34:06 GMT -5
Your doctor is correct. The end result of any of the FOUR (insufficient and not making any are different) is you need more insulin. For T2s the time you really need the insulin is at meal time because this is when it spikes and you need to keep it under 140 or you risk microvascular disease. If your pancreas is still making insulin there is a good chance some or much of the beta cell function can be restored but you have to get your BG back to near normal (80 - 120) give or take for 3 to 6 months. What is your BG 1 hour and 2 hours after eating a low fat high carb meal? Most out of control T2s see it 200+, 300 is atypical. There are a zillion research papers on the reasons for insulin resistance but the end result for the most part is the chicken and egg discussion- did not enough insulin cause the resistance or did the resistance cause glucose toxicity which killed the beta cells. What is usually true is if you get your A1c into the 5s your insulin resistance will not be what it was AND you will most likely get some beta cell function back. We have 40+ years of research papers saying early insulin intervention results in a reversal of diabetes in T2s. Get it back to 5.0 and you are really in business. Also the more muscle mass you can build the more your resistance will lower. Afrezza, moderate carb and moderate-lower fat meal and some exercising - nice walk a couple miles a day- nothing crazy, will get most people in the 5's. Also when your BG spikes it seems the magic number is 180 where the body incurs temporary insulin resistance as a protective measure. Thats why if you watch some of the afrezza users in their youtubes they talk about needing more afrezza when they did not blunt the spike or forgot. Now, the problem for most T2s with the liver producing too much glucose is they have lost first phase insulin release at meal time and the liver is still dumping glucose into the blood. If you have normal phase one release this will shut off the liver. Diabetes is really an engineering flow control problem which Dr. Bernstein who was an engineer not a doctor at the time realized 30 years ago. Basically the liver, pancreas and other organs are out of sync because of high BG and its impacts. High sugars cause so many issues because its a funny thing about the blood, it just seems to be needed by the entire body. So to fix the liver issue you need to get your phase one insulin release back. There are currently only two ways to do this; a healthy pancreas; or a puff of afrezza. No other insulin or insulin analog not even the new Fiasp can provide this function which is critical. The liver needs that big robust hit. Metformin does limit insulin liver glucose production but not in a natural way and causes other issues. For example, 50% of metformin users are now developing Alzheimer's. The biggest thing is it does not address the root T2 issue - stopping the meal time BG spike. Hope this helps. Thank you for your reply. This is one of the reasons I enjoy reading this board. I try to restrict my carb intake to 60 grams per meal. I try to stay compliant 80% of the time. I admit that I do not check my BG after I indulge in a large bowl of ice cream or eat more pizza than I should. I have no doubt it would be between 200 - 300. I take Metformin like most T2's. I take once weekly Trulicity since my insurance no longer covers Bydureon. A side affect of a GLP-1 is that it suppresses appetite. I do a lot of walking and dropped 41# over the years. My A1c stays between 5.6 - 5.8 and I have it checked twice a year. I was told that almost all T2's will become insulin dependent if they live long enough. Do you think Afrezza is appropriate for T2's who are not insulin dependent? My doctor (Internal Medicine) says no. Then again, she said that knowing it is insulin but has not been educated on the drug. Even more amazing is that this clinic is part of the same system that includes The International Diabetes Center in Minneapolis and is in the same building. I was told that her department does not see pharma reps. Pretty hard to get doctors on board when they aren't exposed to what is new on the market. I have been surprised by Minneapolis. When Sanofi was still marketing Afrezza, I called the endocrinology groups around the university campus. I called the u of m endocrinology department. Non of them were prescribing afrezza. The witch that I am decided for all the big talk and thinking in Minneapolis, that we are smarter than the average bear... that our physicians were letting us down. Reimbursement and all. Funding and all. Donors and all. None of the endocrinology desks I spoke with knew about afrezza. Sanofi was marketing Afrezza when I made the calls. I was surprised. I thought in medical groups one of the physicians would keep up as far as studying/assessing the new medications for the group.
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Post by sayhey24 on Jun 11, 2017 7:53:43 GMT -5
Your doctor is correct. The end result of any of the FOUR (insufficient and not making any are different) is you need more insulin. For T2s the time you really need the insulin is at meal time because this is when it spikes and you need to keep it under 140 or you risk microvascular disease. If your pancreas is still making insulin there is a good chance some or much of the beta cell function can be restored but you have to get your BG back to near normal (80 - 120) give or take for 3 to 6 months. What is your BG 1 hour and 2 hours after eating a low fat high carb meal? Most out of control T2s see it 200+, 300 is atypical. There are a zillion research papers on the reasons for insulin resistance but the end result for the most part is the chicken and egg discussion- did not enough insulin cause the resistance or did the resistance cause glucose toxicity which killed the beta cells. What is usually true is if you get your A1c into the 5s your insulin resistance will not be what it was AND you will most likely get some beta cell function back. We have 40+ years of research papers saying early insulin intervention results in a reversal of diabetes in T2s. Get it back to 5.0 and you are really in business. Also the more muscle mass you can build the more your resistance will lower. Afrezza, moderate carb and moderate-lower fat meal and some exercising - nice walk a couple miles a day- nothing crazy, will get most people in the 5's. Also when your BG spikes it seems the magic number is 180 where the body incurs temporary insulin resistance as a protective measure. Thats why if you watch some of the afrezza users in their youtubes they talk about needing more afrezza when they did not blunt the spike or forgot. Now, the problem for most T2s with the liver producing too much glucose is they have lost first phase insulin release at meal time and the liver is still dumping glucose into the blood. If you have normal phase one release this will shut off the liver. Diabetes is really an engineering flow control problem which Dr. Bernstein who was an engineer not a doctor at the time realized 30 years ago. Basically the liver, pancreas and other organs are out of sync because of high BG and its impacts. High sugars cause so many issues because its a funny thing about the blood, it just seems to be needed by the entire body. So to fix the liver issue you need to get your phase one insulin release back. There are currently only two ways to do this; a healthy pancreas; or a puff of afrezza. No other insulin or insulin analog not even the new Fiasp can provide this function which is critical. The liver needs that big robust hit. Metformin does limit insulin liver glucose production but not in a natural way and causes other issues. For example, 50% of metformin users are now developing Alzheimer's. The biggest thing is it does not address the root T2 issue - stopping the meal time BG spike. Hope this helps. Thank you for your reply. This is one of the reasons I enjoy reading this board. I try to restrict my carb intake to 60 grams per meal. I try to stay compliant 80% of the time. I admit that I do not check my BG after I indulge in a large bowl of ice cream or eat more pizza than I should. I have no doubt it would be between 200 - 300. I take Metformin like most T2's. I take once weekly Trulicity since my insurance no longer covers Bydureon. A side affect of a GLP-1 is that it suppresses appetite. I do a lot of walking and dropped 41# over the years. My A1c stays between 5.6 - 5.8 and I have it checked twice a year. I was told that almost all T2's will become insulin dependent if they live long enough. Do you think Afrezza is appropriate for T2's who are not insulin dependent? My doctor (Internal Medicine) says no. Then again, she said that knowing it is insulin but has not been educated on the drug. Even more amazing is that this clinic is part of the same system that includes The International Diabetes Center in Minneapolis and is in the same building. I was told that her department does not see pharma reps. Pretty hard to get doctors on board when they aren't exposed to what is new on the market. You ask - Do you think Afrezza is appropriate for T2's who are not insulin dependent? My doctor (Internal Medicine) says no. My response - in simply words your doctor is very wrong on this. ALL T2s are insulin deficient, by definition. That's the problem. They are not making enough insulin and their pancreas needs help. As CGMs become the norm with things like the Apple watch it will become common knowledge how wrong the current ADA step program is. We have 40+ years of studies saying to treat with insulin asap and that was when we had bad insulins. Now we have a great insulin. You see afrezza basically obsoletes everything your doctor has been taught about treating T2 diabetics. They knew this back in the 1920's when they tried to create the first inhaled insulin. Dr. Bruce Bode presented a few weeks ago at a Medscape educational session and said ALL T2s should be put on afrezza within a year or two of diagnosis. Too bad your doctor is not taking this type of continuing education. Dr. Bode out of Atlanta is one of the leading endo's in the country. I can't blame your doctor for not seeing the Pharma reps. Have her look at the Dr Edelman youtubes, if nothing else. My PCP who is very nice tried to put me on metformin when I got the call about my FBG. I said no and outlined the program for her we would follow. I disagree with Dr. Bode in I say day one put everyone on afrezza although I think he is giving time for diet and exercise. Today I am not taking any meds and post meal 2 hour are under 130 and FBG is around 90 and no special meals. Better if I take a little bourbon before bed. Not bad for someone who saw both my father and grandmother slowly killed by diabetes and thought "Oh No, here we go" when I got the call. Tell your doctor afrezza is not her grandmother's insulin, nor just another analog. It is not another Frankenstein analog. Afrezza is the exact same monomer insulin molecule which is secreted by the pancreas. It is not magic but rather the molecule natural to the human body. It is what the body has evolved to expect. That is why it profiles exactly the same as pancreatic secreted insulin. It is also the reason you do not have the risk of hypos which you do with other insulins - its in/out like pancreatic insulin. Now, don't get me wrong its possible to get a hypo but you really have to work at it. We saw a person dosing 30 minutes before eating and then not eating for an hour and then complaining she got a hypo - good grief. Take it 10 minutes after starting to eat and the chance of a hypo is slim to none as long as your liver is healthy and you discontinue metformin which will effect the liver. The liver will save you from a hypo with afrezza. There are a number of myths with T2 diabetes but one of the bigger ones is that it has to be progressive. If you keep your A1c in the 5's it is usually not progressive but A1c does not tell the story. Its really about meal time spikes and how fast you can get back under 100 after a meal. Microvascular damage is the big thing; heart; eyes; etc. You want to be below 100 within 3 hours but the sooner the better and you really want to stay under 140, but 130 is better 1-2 hours after eating. There was just that article in STAT about Mattock's new show and they referenced the "Study" which "proved" T2's could not be reversed. Well if you look at the study they feed these people high carb low fat diets and no meal time insulin and they saw no improvement - no kidding. The only thing that study proved was high carb meals without afrezza is not a good idea. For newly diagnosed T2 get your A1c close to 5 for 3 to 6 months and most shorter term T2s will see at least some beta cell recovery. Prior to afrezza there were not good options. Metformin does not address the biggest issue, meal time spikes and drugs like Trulicity are even worse. It works by slowing gastric emptying and increases insulin secretion by pancreatic beta cells. This is the last thing you want to do. You want to rest the beta cells not make them work harder. With an A1c of 5.6 - 5.8 your A1c is great but I suspect its mostly because of the 60 carbs which is hard to do. At first I thought you said for an entire day and thought you to be a Bernstein disciple. If you have not had one lately I would suggest you have your doctor give you a glucose tolerance test - you may want to also do this at home prior so you know the numbers going in. Then both you and she can see how you are reacting and maybe she will then take time to learn about afrezza. A good place to start afrezzajustbreathe.com |
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Post by Deleted on Jun 11, 2017 9:07:56 GMT -5
Is there a scientific explanation for "insulin resistance" or is this theory similar to "pancreatic phase response"?
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Post by peppy on Jun 11, 2017 9:45:53 GMT -5
Is there a scientific explanation for "insulin resistance" or is this theory similar to "pancreatic phase response"? multiple patterns of insulin response? Ivor Cummins - 'The Pathways of Insulin Resistance: Exposure and Implications' www.youtube.com/watch?v=U_Gcq8bEUq8
--------------------------------------------------------------------------------------------------------------------------------------- Insulin Resistance
First and second phase insulin release may fail to do their jobs for several reasons. The most common is a condition called insulin resistance in which some receptors in the liver and the muscle cells stop responding properly to insulin. This means that though there is lots of insulin circulating in the body, the muscles and liver (but not, alas, the fat cells) don't respond until the insulin levels rise much higher.
So when a person's cells become insulin resistant, it will take a lot more insulin than usual to push circulating glucose into cells. In this case, while a person might have a perfectly normal first and second phase insulin response, the first phase response might not produce enough insulin to clear the circulating blood glucose resulting from eating a high carbohydrate meal. Then the second phase response might be prolonged because it takes a long time for beta-cells to secrete of the large amounts of insulin needed to counter the insulin resistance. Eventually the body may not be able to produce enough insulin to clear all the dietary carbohydrate from the bloodstream and blood sugars will rise to abnormal levels.
If your beta-cells are normal, and if insulin resistance at the muscles and liver is your only problem, over time you may be able to grow new pancreas islets filled with new beta-cells that can store even more insulin for use in first and second phase insulin response. In this case, though your blood sugar may continue to rise into the impaired range and take longer than normal to go back down to normal levels, your blood sugar response may never deteriorate past the impaired glucose tolerance stage to full-fledged diabetes. This is what happens to most people who have what is called "Metabolic Syndrome." Unfortunately, if you have impaired glucose tolerance, there is no way of knowing if you fall into this group or if your rising blood sugars are caused by failing or dying beta-cells.
Read more: mnkd.proboards.com/thread/3407/blood-sugar-101-tell-diabetes#ixzz4jhmPoCbD ----------------------------------------------------------------------------------------------------------------------------------------------------------
I just figured the cells were too pooped to pop. 
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