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Post by ktim on Dec 11, 2019 12:33:43 GMT -5
Yes, it echos MNKD's own talking points, and indeed the argument was what got me to invest in MNKD, as well as knowing of Al and knowing people that worked with him. This article doesn't address swapping prandial for basal in treatment progression, however. Ah, if only that high worldwide demand they predicted 5 1/2 years ago had come to fruition quicker. |
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Post by ktim on Dec 11, 2019 13:51:24 GMT -5
It's usually obvious you aren't in science. Designed experiments are the basis of science. Anyway, short of directing you to your nearest local university to have someone that does scientific research explain it to you, I think we've come to an impasse. Blindly believing in your deductive intuition is folly within science. Though, as stated multiple times my intuition aligns with yours in this case, just being a scientist I know the difference between deductive intuition and proven science. No, I am not a scientist but that doesn’t mean I can’t understand a concept. I don’t blindly believe in my “deductive intuition” as you claim. I believe the research I have read over the years makes logical, common sense and can easily agree with the late particle physicist and diabetes pioneer and innovator, Alfred E. Mann, that basal insulin for T2D is medically incorrect. 😉 What we do know is that people who get put on basal insulin for T2D always gets worse. Makes logical sense considering it has nothing to do with the first-phase and so the disease just continually progresses. I believe you're confusing him for the other physicist named Alfred Mann (middle initial K). Mannkind's Mann wasn't a particle physicist. He did research in solid state physics. That's related to my field so familiar with his work. If Mannkind produces data to show Afrezza halts diabetes progression, that would certainly be a huge game changer. As yet, no experimental data show that. Perhaps I should substitute "logical sense" for "deductive intuition" since you seem to prefer that terminology. Not sure about how blind you accept it, but you don't seem to think confirming "logical senses" about scientific ideas with controlled experiments is part of the scientific process. Especially in pharmaceuticals many ideas that make logical sense turn out to simply be wrong. Things that seem promising initially that simply don't behave in the body as they seem they might or should. Drug companies wouldn't spend billions on drug discovery if logical sense was all that was needed to develop treatments. One does have different perspective from working in a scientific field where one must learn to purposely and constantly question these "logical senses" and make sure when testing them one isn't unconsciously engaging in confirmation bias. The idea that Afrezza might slow progression more than other insulin regimes is an intriguing one and the potential of it was part of what led me to invest in MNKD. |
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Post by harryx1 on Dec 11, 2019 14:17:54 GMT -5
A gif is worth $10 Billion....  |
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Post by brentie on Dec 11, 2019 14:26:01 GMT -5
Yes, it echos MNKD's own talking points, and indeed the argument was what got me to invest in MNKD, as well as knowing of Al and knowing people that worked with him. This article doesn't address swapping prandial for basal in treatment progression, however.
Ah, if only that high worldwide demand they predicted 5 1/2 years ago had come to fruition quicker. I think it does... " In type 2 patients, the first insulin problem is the loss of the first phase insulin release, so inhaling Afrezza should be a great treatment to overcome that physiologic defect in early type 2. For those with more advanced type 2, taking a basal insulin like Lantus or Levemir, adding Afrezza would greatly improve after meal elevations." |
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Post by sayhey24 on Dec 11, 2019 19:25:43 GMT -5
No, I am not a scientist but that doesn’t mean I can’t understand a concept. I don’t blindly believe in my “deductive intuition” as you claim. I believe the research I have read over the years makes logical, common sense and can easily agree with the late particle physicist and diabetes pioneer and innovator, Alfred E. Mann, that basal insulin for T2D is medically incorrect. 😉 What we do know is that people who get put on basal insulin for T2D always gets worse. Makes logical sense considering it has nothing to do with the first-phase and so the disease just continually progresses. I believe you're confusing him for the other physicist named Alfred Mann (middle initial K). Mannkind's Mann wasn't a particle physicist. He did research in solid state physics. That's related to my field so familiar with his work. If Mannkind produces data to show Afrezza halts diabetes progression, that would certainly be a huge game changer. As yet, no experimental data show that. Perhaps I should substitute "logical sense" for "deductive intuition" since you seem to prefer that terminology. Not sure about how blind you accept it, but you don't seem to think confirming "logical senses" about scientific ideas with controlled experiments is part of the scientific process. Especially in pharmaceuticals many ideas that make logical sense turn out to simply be wrong. Things that seem promising initially that simply don't behave in the body as they seem they might or should. Drug companies wouldn't spend billions on drug discovery if logical sense was all that was needed to develop treatments. One does have different perspective from working in a scientific field where one must learn to purposely and constantly question these "logical senses" and make sure when testing them one isn't unconsciously engaging in confirmation bias. The idea that Afrezza might slow progression more than other insulin regimes is an intriguing one and the potential of it was part of what led me to invest in MNKD. Brentie - Brilliant article. I am not sure I had seen this before but if I did I certainly forgot. Keith Campbell's death was another huge lose in the diabetes community. ktim - the last I checked Al did more than research in solid state physics. He figured out how to take Bell Lab's research in solar cells and make them work as solar panels which formed the foundation for Spectrolabs. I think it would be fair to say without Al the future of solar panels was in jeopardy. As far as showing afrezza benefits "even leads to lower fasting levels" Al discussed this in 3Q2009 quarterly call the 118 study - see below. Dr. Kendall has the study. More recently there was a study by the Model Clinical Research (MCR) center. It was suppose to wrap up end of September. Maybe its one Mike mentioned last week for February presentation. Here is a little write-up www.type2nation.com/treatment/could-early-intensive-insulin-therapy-be-a-breakthrough-t2d-treatment/Study info is here - clinicaltrials.gov/ct2/show/NCT03324776Mango - thanks for explaining how diabetes should be treated. Its hard for me to believe we still need to have this discussion but its so much easier these days when you can hook up a T2 to a CGM and let them watch their post meal spike at 200+ and then not let them eat again until they are back to Dr. Bernstein's 87 mg/dl. Its not surprising most never get there until they get the afrezza. When they understand their non-diabetics friends seldom go above 130 and are back to Bernstein's 87 in about 2 hours they usually get the message especially the metformin users. The best part is anyone can do this "trial" by making a trip to Walmart and getting the Libre and afrezza. Then again my favorite quote of all time “The most waste in type 2 diabetes is to continuously put people on metformin and sulfonylureas (glyburide, glimepiride, etc.). These drugs have no protective effect on the beta cell, and by the time you figure out what you’re doing, there are no beta cells left to save.” – Dr. Ralph DeFronzo (University of Texas Health Science Center) diatribe.org/the-diatribe-foundation-and-tcoyd-11th-annual-forumkitm - Per the 3Q2009 Quarterly call (with the original spelling of afrezza and I still have my t-shirt!) Al Mann said - I have long argued that AFRESA does not require complex meal titration. Certainly there is no need for carb counting and so forth. The basis of my view was derived from the dose escalation study with meal challenges in which better glucose control was achieved with ever greater doses of AFRESA, yet without any hypos. Yet based on decades of battling these challenges of conventional insulin therapy, some physicians have questioned my suggestion. Therefore, I proposed a meal escalation study in which patients would take a fixed dose of AFRESA and then a series of meal challenges. Our clinical team designed a protocol to set a standard meal with 50 g of carbohydrates. That was the 100% challenge. This was followed by challenges at 200%, 50% and zero percent. When I heard of zero I was shocked. Surely there would be severe hypo. The remarkable thing was that with the regular prescribed dose of AFRESA regardless of carbohydrate intake between zero and 100 grams the range of excursion is only plus or minus 30-35 mg [reduction] from baseline for all of the Type II patients in the study. At the ASDA meeting I described to Dr. [Jay Skyler] the finding that in Type II diabetes with a fixed dose of AFRESA and even with no food there is excellent control without hypo risk. I asked him how that was possible. "Obvious," he responded. He was basing his comments on our recently reported 118 trial in which we showed rapid and virtually complete sensation of [hepatic] glucose relief with AFRESA and the common inability of the remaining endogenous insulin to maintain control, as is the case for a healthy person without diabetes. Indeed, I mentioned this result to a number of KOL's who agree with Jay. So I say to you that AFRESA is what no other insulin has ever done for Type II diabetes. AFRESA restores more physiologic hepatic function, takes a load off the pancreas and avoids the hyperinsulinemia resulting from resistance of other insulins. It better mimics the normal pancreas response. So what does all this mean? First let me say that we will need to follow these findings with much larger trials. If the results of the larger trials support the earlier findings then I state to you that AFRESA should be used very early, certainly after failure with Metformin and as a first sign therapy for a significant portion of patients who are not candidates for Metformin or who do not do well with Metformin. It should be used well before fasting glucose is out of control and as we have seen, AFRESA even leads to lower fasting levels by eliminating the excessive gluconeogenesis. Of course, we will have to repeat some of these findings with specific trials but we have already seen the possibilities for AFRESA as we evaluate the timing of hypos in our already completed trials to date. From what we have seen in our extensive clinical program, AFRESA should benefit the entire progression spectrum of Type II diabetes with a very simple therapy and the experts tell us that it could even stop the progression of the disease.
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Post by mango on Dec 11, 2019 21:04:07 GMT -5
I believe you're confusing him for the other physicist named Alfred Mann (middle initial K). Mannkind's Mann wasn't a particle physicist. He did research in solid state physics. That's related to my field so familiar with his work. If Mannkind produces data to show Afrezza halts diabetes progression, that would certainly be a huge game changer. As yet, no experimental data show that. Perhaps I should substitute "logical sense" for "deductive intuition" since you seem to prefer that terminology. Not sure about how blind you accept it, but you don't seem to think confirming "logical senses" about scientific ideas with controlled experiments is part of the scientific process. Especially in pharmaceuticals many ideas that make logical sense turn out to simply be wrong. Things that seem promising initially that simply don't behave in the body as they seem they might or should. Drug companies wouldn't spend billions on drug discovery if logical sense was all that was needed to develop treatments. One does have different perspective from working in a scientific field where one must learn to purposely and constantly question these "logical senses" and make sure when testing them one isn't unconsciously engaging in confirmation bias. The idea that Afrezza might slow progression more than other insulin regimes is an intriguing one and the potential of it was part of what led me to invest in MNKD. Brentie - Brilliant article. I am not sure I had seen this before but if I did I certainly forgot. Keith Campbell's death was another huge lose in the diabetes community. ktim - the last I checked Al did more than research in solid state physics. He figured out how to take Bell Lab's research in solar cells and make them work as solar panels which formed the foundation for Spectrolabs. I think it would be fair to say without Al the future of solar panels was in jeopardy. As far as showing afrezza benefits "even leads to lower fasting levels" Al discussed this in 3Q2009 quarterly call the 118 study - see below. Dr. Kendall has the study. More recently there was a study by the Model Clinical Research (MCR) center. It was suppose to wrap up end of September. Maybe its one Mike mentioned last week for February presentation. Here is a little write-up www.type2nation.com/treatment/could-early-intensive-insulin-therapy-be-a-breakthrough-t2d-treatment/Study info is here - clinicaltrials.gov/ct2/show/NCT03324776Mango - thanks for explaining how diabetes should be treated. Its hard for me to believe we still need to have this discussion but its so much easier these days when you can hook up a T2 to a CGM and let them watch their post meal spike at 200+ and then not let them eat again until they are back to Dr. Bernstein's 87 mg/dl. Its not surprising most never get there until they get the afrezza. When they understand their non-diabetics friends seldom go above 130 and are back to Bernstein's 87 in about 2 hours they usually get the message especially the metformin users. The best part is anyone can do this "trial" by making a trip to Walmart and getting the Libre and afrezza. Then again my favorite quote of all time “The most waste in type 2 diabetes is to continuously put people on metformin and sulfonylureas (glyburide, glimepiride, etc.). These drugs have no protective effect on the beta cell, and by the time you figure out what you’re doing, there are no beta cells left to save.” – Dr. Ralph DeFronzo (University of Texas Health Science Center) diatribe.org/the-diatribe-foundation-and-tcoyd-11th-annual-forumkitm - Per the 3Q2009 Quarterly call (with the original spelling of afrezza and I still have my t-shirt!) Al Mann said - I have long argued that AFRESA does not require complex meal titration. Certainly there is no need for carb counting and so forth. The basis of my view was derived from the dose escalation study with meal challenges in which better glucose control was achieved with ever greater doses of AFRESA, yet without any hypos. Yet based on decades of battling these challenges of conventional insulin therapy, some physicians have questioned my suggestion. Therefore, I proposed a meal escalation study in which patients would take a fixed dose of AFRESA and then a series of meal challenges. Our clinical team designed a protocol to set a standard meal with 50 g of carbohydrates. That was the 100% challenge. This was followed by challenges at 200%, 50% and zero percent. When I heard of zero I was shocked. Surely there would be severe hypo. The remarkable thing was that with the regular prescribed dose of AFRESA regardless of carbohydrate intake between zero and 100 grams the range of excursion is only plus or minus 30-35 mg [reduction] from baseline for all of the Type II patients in the study. At the ASDA meeting I described to Dr. [Jay Skyler] the finding that in Type II diabetes with a fixed dose of AFRESA and even with no food there is excellent control without hypo risk. I asked him how that was possible. "Obvious," he responded. He was basing his comments on our recently reported 118 trial in which we showed rapid and virtually complete sensation of [hepatic] glucose relief with AFRESA and the common inability of the remaining endogenous insulin to maintain control, as is the case for a healthy person without diabetes. Indeed, I mentioned this result to a number of KOL's who agree with Jay. So I say to you that AFRESA is what no other insulin has ever done for Type II diabetes. AFRESA restores more physiologic hepatic function, takes a load off the pancreas and avoids the hyperinsulinemia resulting from resistance of other insulins. It better mimics the normal pancreas response. So what does all this mean? First let me say that we will need to follow these findings with much larger trials. If the results of the larger trials support the earlier findings then I state to you that AFRESA should be used very early, certainly after failure with Metformin and as a first sign therapy for a significant portion of patients who are not candidates for Metformin or who do not do well with Metformin. It should be used well before fasting glucose is out of control and as we have seen, AFRESA even leads to lower fasting levels by eliminating the excessive gluconeogenesis. Of course, we will have to repeat some of these findings with specific trials but we have already seen the possibilities for AFRESA as we evaluate the timing of hypos in our already completed trials to date. From what we have seen in our extensive clinical program, AFRESA should benefit the entire progression spectrum of Type II diabetes with a very simple therapy and the experts tell us that it could even stop the progression of the disease.
Al’s work in photovoltaics and at SpectroLabs was also key to helping NASA during that time when they worked with SpectroLabs during the Cold War under the cover story of studying solar radiation while they were actually launching photoreconnaissance satellites for the DoD (operation GRAB being one). In essence, Al played a key role in helping end the Cold War via his work in photovoltaics. |
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Post by agedhippie on Dec 12, 2019 7:01:49 GMT -5
... So I say to you that AFRESA is what no other insulin has ever done for Type II diabetes. AFRESA restores more physiologic hepatic function, takes a load off the pancreas and avoids the hyperinsulinemia resulting from resistance of other insulins. It better mimics the normal pancreas response. So what does all this mean? First let me say that we will need to follow these findings with much larger trials. If the results of the larger trials support the earlier findings then I state to you that AFRESA should be used very early, certainly after failure with Metformin and as a first sign therapy for a significant portion of patients who are not candidates for Metformin or who do not do well with Metformin. ... I have highlighted the bit that matters in that conversation from the scientific standpoint. Al is talking through the rationale as to why he believes Afrezza works the way it does and then we get to the part in red. Notice " First let me say", that is the tell that this is a theory and not proven. That is followed by " If the results of the larger trial..." which is the acknowledgment that the first trial may have issues and there might be no sustainable change. Now Al undoubtably believed his hypothesis and result, every scientist does at this point or they wouldn't be doing it, but he is a scientist and wants proof - the large scale trials. He wants hard proof to be sure, and that proof is the larger scale trials (note his use of the plural). Without those trials this remains a hypothesis was far as the medical world is concerned. |
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Post by agedhippie on Dec 12, 2019 7:20:34 GMT -5
If anyone wants to see what happens when you over or under dose with Afrezza then this is the only trial that has that data I believe - clinicaltrials.gov/ct2/show/results/NCT00747006. The important bit first; this is a study rather than a trial given the tiny (18) numbers involved and ultimately once they withdrew the Type 1 candidates that was probably why they shut it down. What do you see? In the Type 2 Afrezza group with the original protocol one of the people had a hypo when they halved the carbs so carb counting does matter. With the amended protocol neither the RAA nor Afrezza groups had hypos, and that included the case where they took insulin and did not eat. Now again, these were tiny numbers and you cannot draw a meaningful conclusion, but what you can say is that in at least some cases people on Afrezza had a hypo where they got the carbs wrong, and also that in some cases people can take RAA and not eat without getting a hypo. (As a note here - I am not suggesting this is a good idea, or will happen reliably, just that it has happened and is documented). |
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Post by sportsrancho on Dec 12, 2019 19:17:33 GMT -5
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Post by sayhey24 on Dec 12, 2019 19:25:44 GMT -5
If anyone wants to see what happens when you over or under dose with Afrezza then this is the only trial that has that data I believe - clinicaltrials.gov/ct2/show/results/NCT00747006. The important bit first; this is a study rather than a trial given the tiny (18) numbers involved and ultimately once they withdrew the Type 1 candidates that was probably why they shut it down. What do you see? In the Type 2 Afrezza group with the original protocol one of the people had a hypo when they halved the carbs so carb counting does matter. With the amended protocol neither the RAA nor Afrezza groups had hypos, and that included the case where they took insulin and did not eat. Now again, these were tiny numbers and you cannot draw a meaningful conclusion, but what you can say is that in at least some cases people on Afrezza had a hypo where they got the carbs wrong, and also that in some cases people can take RAA and not eat without getting a hypo. (As a note here - I am not suggesting this is a good idea, or will happen reliably, just that it has happened and is documented). Aged - what I see is a study which was stopped. My first question is why? My second question is 1 out of 8 T2s got a hypo at 50% yet in the 118 none got them at 0%, what is different with that one T2? Could they have a liver issue or maybe the PWDs were not properly screened and this one is taking a TZD or a sulfonylureas. I think in this case it was glyburide but who would ever know thats a sulfonylureas? Clearly not this PWD. It would have made little sense to continue with a tainted patient pool. Don't you agree? As far as following the 118 with a bigger trial, it was. It was called the 175 or Affinity 2. What did that show? Nearly no hypos and better A1c and let me add better A1c even when under dosing afrezza in most cases. Again who had most of the hypos? A single PWD using a TZD. A few other PWD were found to have liver issues but I am not recommending afrezza for diagnostic purposes. What we have learned is the chance of an otherwise healthy T2 getting a severe hypo using afrezza is really damn low. So low, ZERO got them in the 118 trial taking ZERO carbs. The good news is the India trial is getting ready to start. Once complete that should end all future complaints and whining about further studies needed. I am waiting to see who the CGM vendor is. I suspect based on Mike's comments last week it is Dexcom. I hope Dexcom brings their partner Onduo into the study as Onduo just proved in their 700+ PWD study they could only reduce PWDs who were 10+ to 8+ without afrezza. Bring in the afrezza and BOOM. Seven or better here they come. Maybe 6 or better might be more accurate. |
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Post by mango on Dec 12, 2019 20:56:50 GMT -5
Very nice write up! I was wondering what he wrote after reading in his bio that he had written about this. Great work, hopefully not the last either. |
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Post by agedhippie on Dec 13, 2019 12:42:15 GMT -5
If anyone wants to see what happens when you over or under dose with Afrezza then this is the only trial that has that data I believe - clinicaltrials.gov/ct2/show/results/NCT00747006. The important bit first; this is a study rather than a trial given the tiny (18) numbers involved and ultimately once they withdrew the Type 1 candidates that was probably why they shut it down. What do you see? In the Type 2 Afrezza group with the original protocol one of the people had a hypo when they halved the carbs so carb counting does matter. With the amended protocol neither the RAA nor Afrezza groups had hypos, and that included the case where they took insulin and did not eat. Now again, these were tiny numbers and you cannot draw a meaningful conclusion, but what you can say is that in at least some cases people on Afrezza had a hypo where they got the carbs wrong, and also that in some cases people can take RAA and not eat without getting a hypo. (As a note here - I am not suggesting this is a good idea, or will happen reliably, just that it has happened and is documented). Aged - what I see is a study which was stopped. My first question is why? My second question is 1 out of 8 T2s got a hypo at 50% yet in the 118 none got them at 0%, what is different with that one T2? Could they have a liver issue or maybe the PWDs were not properly screened and this one is taking a TZD or a sulfonylureas. I think in this case it was glyburide but who would ever know thats a sulfonylureas? Clearly not this PWD. It would have made little sense to continue with a tainted patient pool. Don't you agree? As far as following the 118 with a bigger trial, it was. It was called the 175 or Affinity 2. What did that show? Nearly no hypos and better A1c and let me add better A1c even when under dosing afrezza in most cases. Again who had most of the hypos? A single PWD using a TZD. A few other PWD were found to have liver issues but I am not recommending afrezza for diagnostic purposes. What we have learned is the chance of an otherwise healthy T2 getting a severe hypo using afrezza is really damn low. So low, ZERO got them in the 118 trial taking ZERO carbs. The good news is the India trial is getting ready to start. Once complete that should end all future complaints and whining about further studies needed. I am waiting to see who the CGM vendor is. I suspect based on Mike's comments last week it is Dexcom. I hope Dexcom brings their partner Onduo into the study as Onduo just proved in their 700+ PWD study they could only reduce PWDs who were 10+ to 8+ without afrezza. Bring in the afrezza and BOOM. Seven or better here they come. Maybe 6 or better might be more accurate. The answer I suspect is the total loss of the Type 1 arm of the trial to hypos when they reduced the carbs. I think there was an expectation that hypos would be mitigated by the speed of action which was not met in that case. That left just they Type 2 arm and even there they had to modify the protocol and wound up with the only hypo being in the Afrezza arm and not the Humalog arm. At that point they cut their losses and closed the trial which was the right thing to do given the cost of these things. If anyone got through the onboarding with a sulfa then the organization running the trial should be shot since they are meant to check all of that. You never rely on the patient. I have been in trials and they go over your drug list with a fine toothed comb. I think the chance is negligible that it was drug influenced. I am not really that impressed with Affinity 2. You take a group that are not well controlled and add insulin to one arm but not the other. It's not hard to see how that ends! Even with underdosing the Afrezza arm should walk that contest. That underdosing will also reduce the chance of hypos since they will run higher glucose levels than they could as can be seen from the average pre-meal levels. I am fairly relaxed about levels, but I wouldn't have been happy with that. The result of the trial I previously posted the link to showed less hypos in the Humalog arm than in the Afrezza arm. It's typically harder for a Type 2 to get a hypo anyway because of insulin resistance (thin Type 2 aside) which attenuates the effect of any excess insulin. Personally I think insulin should be given far far earlier than it is for Type 2, but I understand why it isn't (compliance and patient resistance). I remain skeptical that they will use CGMs but it would be money well spent if they did. If Cipla are paying for the trial there is no reason for them to spend more than is required for to tick the box. |
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Post by sayhey24 on Dec 13, 2019 16:10:05 GMT -5
Aged - Affinty 2 was designed by the FDA. At that point in time MNKD was willing to do anything to get afrezza approved. If nothing else it demonstrated metformin and afrezza had about the same safety profile with the noted exceptions. The bottom line being there is little utility in using metformin when afrezza is available. MNKD now gets a mulligan with India and the ability to use CGMs which in 2014 were not common place. No more guessing with real time cloud reporting. Real AGPs and real time dosing when second and third dosing needed. If they were to add Onduo real time coaching and its game over.
Trying to argue you will get fewer hypos with Humalog is not a discuss I want to have. I am past that point. Humalog has not changed the perception insulin is dangerous- it requires needles and can cause hypos. That is the perception, dangerous. Afrezza holds the potential to change the perception.
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Post by agedhippie on Dec 13, 2019 16:26:26 GMT -5
Aged - Affinty 2 was designed by the FDA. At that point in time MNKD was willing to do anything to get afrezza approved. If nothing else it demonstrated metformin and afrezza had about the same safety profile with the noted exceptions. The bottom line being there is little utility in using metformin when afrezza is available. MNKD now gets a mulligan with India and the ability to use CGMs which in 2014 were not common place. No more guessing with real time cloud reporting. Real AGPs and real time dosing when second and third dosing needed. If they were to add Onduo real time coaching and its game over. Trying to argue you will get fewer hypos with Humalog is not a discuss I want to have. I am past that point. Humalog has not changed the perception insulin is dangerous- it requires needles and can cause hypos. That is the perception, dangerous. Afrezza holds the potential to change the perception. I wouldn't argue that Afrezza is more hypo prone than Humalog, but it shows the sort of anomaly that gets thrown up in small trials and why they are meaningless. When the number of events is small it takes a large sample set to prove results hence my (and the ADA) fixation with trial size. The utility from the medical point of view is compliance and cost. Metformin is not a long term fix in the majority of cases, but initially it's an easy choice for those reasons. |
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Post by sayhey24 on Dec 13, 2019 17:48:35 GMT -5
Aged - it doesn't matter if its one PWD or 1000 PWDs, afrezza with a CGM and second dosing when needed will always win. Who wants to be a human pin cushion? Thats the compliance issue - needles. Taking a puff of afrezza is little different than taking a sip of your favorite drink using a straw. Cost of afrezza is above my pay grade. When it comes to metformin all I can do is quote Ralph DeFronzo the "Father" of metformnin in the U.S. So I will. Too bad it took him 25 years to figure out it was garbage. “The most waste in type 2 diabetes is to continuously put people on metformin and sulfonylureas (glyburide, glimepiride, etc.). These drugs have no protective effect on the beta cell, and by the time you figure out what you’re doing, there are no beta cells left to save.” – Dr. Ralph DeFronzo (University of Texas Health Science Center) diatribe.org/the-diatribe-foundation-and-tcoyd-11th-annual-forum |
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