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Post by mnholdem on Jan 1, 2018 11:57:52 GMT -5
Failing beta-cellsFirst phase insulin release also fails because beta-cells are dysfunctional or dying. This can happen along with insulin resistance, or without it. Studies have found that some thin, non-insulin resistant relatives of people with Type 2 Diabetes already show signs of beta cell dysfunction. If beta-cells are dying or not working properly the remaining beta-cells may be working full-time just to keep up with the need for a basal insulin release so they can't store any excess in those granules for later release. Some people with type 2 diabetes appear to have a defect which makes their beta-cells die when they attempt to reproduce in response to a need for more insulin. For these people, insulin resistance can cause the beta-cells to try to divide and then die, hastening on the degenerative process. It is also possible that some people who develop type 2 diabetes have a genetic defect which prevents their beta-cells from storing insulin though their beta-cells are still capable of secreting it. Scientists have discovered dozens of different genetic defects which cause beta-cells to fail or die in humans and animals. Many genes are expressed in the process that leads to the correct functioning of the beta-cells and many others in the cell receptors which respond to insulin. This means that one person's Type 2 Diabetes can behave quite differently from that of another person, depending on what exactly is broken in their blood sugar control system. This is why drugs that work well for one person may do little for another person. By understanding your own pattern of blood sugar response you may get some insight into what might be malfunctioning in your individual case. Rising Blood Sugar Concentrations Further Damage Your Ability to Produce InsulinGlucose ToxicityWhatever the reason for the failing first phase insulin release there's an ugly feedback mechanism that kicks in when blood sugar levels rise because of that failing first phase insulin release: High levels of circulating glucose themselves are toxic to beta-cells, a phenomenon called "glucose toxicity". So as blood sugars rise these high blood sugar concentrations further damage and or kill more beta-cells, making first and second phase insulin release even less able to control blood sugar concentrations. Increased Insulin ResistanceIf your beta-cells are still able to secrete enough insulin to provide a second phase insulin release, your body may be able to bring the blood sugar back down to a normal level by 3 hours and may then go back to secreting the small amounts of basal insulin which maintain a normal or near-normal blood sugar level while you are between meals or asleep. But when first phase insulin release is weak or missing your blood sugar may easily rise over the 200 mg/dl (11 mmol/L) level currently defined as "diabetes." At that point, two bad things happen. When the concentration of glucose in your blood reaches 200 mg/dl (11 mmol/L) your cells become insulin resistant even if they weren't insulin resistant before, so it takes a lot more insulin to lower your blood sugar from that point on. And, even worse, the lack of a robust insulin response to the rising glucose may erroneously be interpreted by your liver as a sign that blood sugar is too low and that it is time to dump more glucose into the bloodstream. So in addition to the glucose coming in from your recent meal you also have to contend with additional glucose dumped by your poor old confused liver. Read more: mnkd.proboards.com/thread/3407/blood-sugar-101-tell-diabetes?page=1#ixzz52x8WrCWJ
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Post by agedhippie on Jan 1, 2018 12:58:13 GMT -5
Aged - Gary is not only now using afrezza he is also speaking on it. He started soon after his review integrateddiabetes.com/my-review-of-afrezza-fast-acting-inhaled-insulin/ came out. Gary goes way back with Al Mann as he was one of the first Minimed pump users when he was at Joslin. He waited a few years on afrezza to see if the lung FUD was an issue and came to the conclusion it was a lot of FUD. Back in 1920 Goat's Rue was about all they had. When insulin was discovered it 1921 it quickly became obsoleted. Because of the disaster of Orinase and the rest of the T2 meds Goat's Rue was more or less reborn as Metformin. In the U.S. we have guys like Ralph DeFronzo to thank and now 25 years later what does Ralph say about metformin? ... We are testing a lot more now than ever before for antibodies and guess what we are finding? Yes more LADAs who a few years ago we would have called T2s. Now, if we test all T2s and had better testing would more and more T2s show some level of some anitbodies? - my guess is yes but it really doesn't matter. What we do know is if we get these people asap when they still have beta cell function and put them on afrezza and keep them in a non-diabetic range for 3 - 6 months most will see positive beta cell results. That's pretty much what VDex is doing. Get them early and get them on afrezza. What do they say "afrezza first, afrezza always"? I am very interested is seeing their clinical findings. Hopefully they will have them available soon. I know Gary's history and writings on Afrezza, I use Integrated Diabetes myself. Goat's rue and french liliac are the same plant. A lot of non-diabetics have antibodies, there are even studies to see if you can use these to predict Type 1, but the difference is the quantity. Non-diabetics and Type 2s have traces of antibodies, Type 1 and LADA have armies of them. LADA is confused with Type 2 because of the relatively slow onset (the auto-immune system is making a leisurely lunch out of the beta cells unlike with Type 1). Your auto-immune system doesn't care about your glucose levels, it's going to kill those beta cells regardless.
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Post by dreamboatcruise on Jan 2, 2018 12:37:02 GMT -5
Aged - Gary is not only now using afrezza he is also speaking on it. He started soon after his review integrateddiabetes.com/my-review-of-afrezza-fast-acting-inhaled-insulin/ came out. Gary goes way back with Al Mann as he was one of the first Minimed pump users when he was at Joslin. He waited a few years on afrezza to see if the lung FUD was an issue and came to the conclusion it was a lot of FUD. Back in 1920 Goat's Rue was about all they had. When insulin was discovered it 1921 it quickly became obsoleted. Because of the disaster of Orinase and the rest of the T2 meds Goat's Rue was more or less reborn as Metformin. In the U.S. we have guys like Ralph DeFronzo to thank and now 25 years later what does Ralph say about metformin? ... We are testing a lot more now than ever before for antibodies and guess what we are finding? Yes more LADAs who a few years ago we would have called T2s. Now, if we test all T2s and had better testing would more and more T2s show some level of some anitbodies? - my guess is yes but it really doesn't matter. What we do know is if we get these people asap when they still have beta cell function and put them on afrezza and keep them in a non-diabetic range for 3 - 6 months most will see positive beta cell results. That's pretty much what VDex is doing. Get them early and get them on afrezza. What do they say "afrezza first, afrezza always"? I am very interested is seeing their clinical findings. Hopefully they will have them available soon. I know Gary's history and writings on Afrezza, I use Integrated Diabetes myself. Goat's rue and french liliac are the same plant. A lot of non-diabetics have antibodies, there are even studies to see if you can use these to predict Type 1, but the difference is the quantity. Non-diabetics and Type 2s have traces of antibodies, Type 1 and LADA have armies of them. LADA is confused with Type 2 because of the relatively slow onset (the auto-immune system is making a leisurely lunch out of the beta cells unlike with Type 1). Your auto-immune system doesn't care about your glucose levels, it's going to kill those beta cells regardless. Like T1, I have autoimmune thyroid disease. Been taking levothyroxine for decades now. Replacing the hormone does nothing to stop the immune system from relentless attack on the thyroid. My doc years ago basically told me I'd end up with "a lump of scar tissue where your thyroid now is". I assume that's basically the state of things now. Our immune systems are truly amazing, but unfortunately can become confused.
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Post by Deleted on Jan 2, 2018 13:14:19 GMT -5
dreamboatcruise when you consider the vast number of compounds the immune system has to be able to differentiate between self and non-self, I am surprised there are not more immunological conditions. Sorry to hear of yours.
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Post by dreamboatcruise on Jan 2, 2018 13:20:52 GMT -5
dreamboatcruise when you consider the vast number of compounds the immune system has to be able to differentiate between self and non-self, I am surprised there are not more immunological conditions. Sorry to hear of yours. I'm comparatively lucky. This is probably the easiest of all the dozens of autoimmune diseases to live with... now that we have modern medicine. Wouldn't be here without the levothyroxine, but as it is I live with no ill effects what so ever. Thank you pharma industry
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Post by sayhey24 on Jan 2, 2018 18:35:04 GMT -5
Aged - Gary is not only now using afrezza he is also speaking on it. He started soon after his review integrateddiabetes.com/my-review-of-afrezza-fast-acting-inhaled-insulin/ came out. Gary goes way back with Al Mann as he was one of the first Minimed pump users when he was at Joslin. He waited a few years on afrezza to see if the lung FUD was an issue and came to the conclusion it was a lot of FUD. Back in 1920 Goat's Rue was about all they had. When insulin was discovered it 1921 it quickly became obsoleted. Because of the disaster of Orinase and the rest of the T2 meds Goat's Rue was more or less reborn as Metformin. In the U.S. we have guys like Ralph DeFronzo to thank and now 25 years later what does Ralph say about metformin? ... We are testing a lot more now than ever before for antibodies and guess what we are finding? Yes more LADAs who a few years ago we would have called T2s. Now, if we test all T2s and had better testing would more and more T2s show some level of some anitbodies? - my guess is yes but it really doesn't matter. What we do know is if we get these people asap when they still have beta cell function and put them on afrezza and keep them in a non-diabetic range for 3 - 6 months most will see positive beta cell results. That's pretty much what VDex is doing. Get them early and get them on afrezza. What do they say "afrezza first, afrezza always"? I am very interested is seeing their clinical findings. Hopefully they will have them available soon. I know Gary's history and writings on Afrezza, I use Integrated Diabetes myself. Goat's rue and french liliac are the same plant. A lot of non-diabetics have antibodies, there are even studies to see if you can use these to predict Type 1, but the difference is the quantity. Non-diabetics and Type 2s have traces of antibodies, Type 1 and LADA have armies of them. LADA is confused with Type 2 because of the relatively slow onset (the auto-immune system is making a leisurely lunch out of the beta cells unlike with Type 1). Your auto-immune system doesn't care about your glucose levels, it's going to kill those beta cells regardless. Thats awesome you know Gary and are using IDS. I know you had mentioned in the past that you had used them but I was not aware you still do. There are a number of afrezza prescribing docs down the street from IDS. Now that Gary is using it maybe you are ready to give it a try? Maybe, someone can get you in touch with VDex and you could give them a spin? I would really like to hear of your personal experience and results with them. In fact, if your experience is as positive as others report that IMO would be good cause to go all in on MNKD.
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Post by victoria on Jan 2, 2018 19:13:55 GMT -5
Message to Vdex: could you consider issuing bonds, perhaps, or even stock? Ill bet lots of mnkd investors would want to support your efforts.
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Post by centralcoastinvestor on Jan 2, 2018 20:02:11 GMT -5
Failing beta-cellsFirst phase insulin release also fails because beta-cells are dysfunctional or dying. This can happen along with insulin resistance, or without it. Studies have found that some thin, non-insulin resistant relatives of people with Type 2 Diabetes already show signs of beta cell dysfunction. If beta-cells are dying or not working properly the remaining beta-cells may be working full-time just to keep up with the need for a basal insulin release so they can't store any excess in those granules for later release. Some people with type 2 diabetes appear to have a defect which makes their beta-cells die when they attempt to reproduce in response to a need for more insulin. For these people, insulin resistance can cause the beta-cells to try to divide and then die, hastening on the degenerative process. It is also possible that some people who develop type 2 diabetes have a genetic defect which prevents their beta-cells from storing insulin though their beta-cells are still capable of secreting it. Scientists have discovered dozens of different genetic defects which cause beta-cells to fail or die in humans and animals. Many genes are expressed in the process that leads to the correct functioning of the beta-cells and many others in the cell receptors which respond to insulin. This means that one person's Type 2 Diabetes can behave quite differently from that of another person, depending on what exactly is broken in their blood sugar control system. This is why drugs that work well for one person may do little for another person. By understanding your own pattern of blood sugar response you may get some insight into what might be malfunctioning in your individual case. Rising Blood Sugar Concentrations Further Damage Your Ability to Produce InsulinGlucose ToxicityWhatever the reason for the failing first phase insulin release there's an ugly feedback mechanism that kicks in when blood sugar levels rise because of that failing first phase insulin release: High levels of circulating glucose themselves are toxic to beta-cells, a phenomenon called "glucose toxicity". So as blood sugars rise these high blood sugar concentrations further damage and or kill more beta-cells, making first and second phase insulin release even less able to control blood sugar concentrations. Increased Insulin ResistanceIf your beta-cells are still able to secrete enough insulin to provide a second phase insulin release, your body may be able to bring the blood sugar back down to a normal level by 3 hours and may then go back to secreting the small amounts of basal insulin which maintain a normal or near-normal blood sugar level while you are between meals or asleep. But when first phase insulin release is weak or missing your blood sugar may easily rise over the 200 mg/dl (11 mmol/L) level currently defined as "diabetes." At that point, two bad things happen. When the concentration of glucose in your blood reaches 200 mg/dl (11 mmol/L) your cells become insulin resistant even if they weren't insulin resistant before, so it takes a lot more insulin to lower your blood sugar from that point on. And, even worse, the lack of a robust insulin response to the rising glucose may erroneously be interpreted by your liver as a sign that blood sugar is too low and that it is time to dump more glucose into the bloodstream. So in addition to the glucose coming in from your recent meal you also have to contend with additional glucose dumped by your poor old confused liver. Read more: mnkd.proboards.com/thread/3407/blood-sugar-101-tell-diabetes?page=1#ixzz52x8WrCWJ Mnholdem, this was a very interesting read. I have a friend that has prediabetes. She is a nutritionist and has perfect weight, yet still has prediabetes. It runs in her family. Do you have an article that I could give to her that more fully explains what you posted above and how Afrezza could in fact slow or reverse the destruction of beta cells? I know there have been dozens of posts on this subject but I thought you might be able to get to it quicker than I. Or is the VDex white paper the best document to use? Thanks in advance.
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Post by mnholdem on Jan 2, 2018 21:57:17 GMT -5
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Post by centralcoastinvestor on Jan 2, 2018 23:30:39 GMT -5
Thanks a bunch! I really appreciate it.
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Post by hellodolly on Jan 3, 2018 6:32:50 GMT -5
dreamboatcruise when you consider the vast number of compounds the immune system has to be able to differentiate between self and non-self, I am surprised there are not more immunological conditions. Sorry to hear of yours. I'm comparatively lucky. This is probably the easiest of all the dozens of autoimmune diseases to live with... now that we have modern medicine. Wouldn't be here without the levothyroxine, but as it is I live with no ill effects what so ever. Thank you pharma industry Ha! I'm cruising on the same boat as 'Dreamboat". I've been TAKING THE levothyroxine SINCE 1992. Miracle drug. Mine were nuked.
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Post by sayhey24 on Jan 3, 2018 6:35:03 GMT -5
Thanks a bunch! I really appreciate it. What should be noted is they were not using afrezza in these studies. The biggest thing is stopping the after meal spike and getting her back to non-diabetic numbers asap. If these studies used afrezza I suspect they would have had even greater success. The first thing I would have her do is get a script for an Abbott libre and have her collect here 24/7 BG profile for the next 2 weeks while keeping a food log.
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Post by dh4mizzou on Jan 3, 2018 7:41:47 GMT -5
It certainly seems like VDEX is a clear positive for Afrezza. It would be great if they had one on every street corner in America. You know, like CVS and Walgreens ;-)
Serious question though. Why is VDEX not negotiating with places like CVS to provide space in their stores for VDEX offices? Heck they already have nurse-practitioners in them.
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Post by hellodolly on Jan 3, 2018 8:41:46 GMT -5
It certainly seems like VDEX is a clear positive for Afrezza. It would be great if they had one on every street corner in America. You know, like CVS and Walgreens ;-) Serious question though. Why is VDEX not negotiating with places like CVS to provide space in their stores for VDEX offices? Heck they already have nurse-practitioners in them. Not their business model? From what the VDEX poster has brought to the boards, it reads like they are heading in the direction of opening up one clinic at a time (as they get franchisee's to buy in). JMHO.
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Post by sportsrancho on Jan 3, 2018 9:28:04 GMT -5
They have three models, their own standalone, other people opening up their own Vdex’s with their help, and smaller Vdex’s inside medical facilities. .
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