|
|
Post by sophie on Jul 2, 2018 10:11:44 GMT -5
I wonder if you all are as vigilant with the rest of your lives as you are about Afrezza and glucose control. I wonder if you all stick to a rigid diet of lean meats and 3-4 servings of fruits and vegetables daily. Then rigorously exercise for at least an hour a day.
Taking care of one's self is a great thing to do. However, when it becomes as obsessive and intrusive as some on the board make it to be, they miss out on the big picture. Their lives no longer become more simplified, rather it becomes more stressful. And I'm not talking about the ease of use of Afrezza as there is not an easier route than pop, click, inhale. What I'm speaking to is the psychological stress some on this board seem to impose on themselves or others when their thinking becomes obsessive.
Aged has found something that works well for him/her. Instead of applauding and encouraging the health he/she has found, you all dissect down to the smallest component and obsess over it. That's not the way to win people over, nor is it the way that the real world works. Any doctor would be overjoyed with Aged's results of 6.5% and would likely not change a thing, especially if the patient was content with the results. It doesn't always matter if better exists. There is such thing as good enough, which many of you won't learn on WebMD. It's why there are so many different treatment options. You pick the one that works best for each person, not the one that works best in a study or has the most potential for health. Compliance is so difficult to attain that it's considered a win to get to 6.5%, regardless of the path to get there.
Many of you will hear me attacking Afrezza and being a "basher" or some other nonsense. I think Afrezza is the best insulin on the market and should be the go to meal-time insulin. It's sometimes difficult to read such strong opinions from people who have no experience outside of a textbook, medical journal, or website. Unfortunately, their arguments seem to pervade the rest of the board, leading to false expectations and just a general misunderstanding of how the real world works.
|
|
|
|
Post by uvula on Jul 2, 2018 10:20:24 GMT -5
Read the bottom of the graph. "relative risk set to 1 for HbA1c of 6%". The curve doesn't go flat at 6. The curve stops at 6 because that is how they chose to represent the data. Aged's point is still valid. There is a point of diminishing returns.
|
|
|
|
Post by agedhippie on Jul 2, 2018 12:39:04 GMT -5
Thiat is why I don't stress the whole getting to non-diabetic numbers thing. Although lowering your A1c by 1.0 halves your risk by the time you get below 6.5 (or pretty much below 7.0) if you look at the graph for complications below you see that the curve goes flat so you are halving a very small number and in real terms that means that there is no difference to the real risk. You need to look at the data and not the headline numbers.  you are halving a relative number so you dont know if it is a small number or not. If at 6=2000 problems, then at 7=4000 and on that case, thats a lot. Your Graph dont show the absolut numbers si how can you say that its small? The gradient of the curve is what matters. If the gradient is small then the increase in risk is small and the incidence of complications will be virtually unchanged. That is the small number that matters. In theory a relative risk of 1 is the same risk as a non-diabetic person in 1996 when this data was collected, and since diabetic complications in that population are virtually nil then even doubling the risk represents a minimal increase in complications in real terms. |
|
|
|
Post by mango on Jul 2, 2018 13:13:14 GMT -5
I wonder if you all are as vigilant with the rest of your lives as you are about Afrezza and glucose control. I wonder if you all stick to a rigid diet of lean meats and 3-4 servings of fruits and vegetables daily. Then rigorously exercise for at least an hour a day. Taking care of one's self is a great thing to do. However, when it becomes as obsessive and intrusive as some on the board make it to be, they miss out on the big picture. Their lives no longer become more simplified, rather it becomes more stressful. And I'm not talking about the ease of use of Afrezza as there is not an easier route than pop, click, inhale. What I'm speaking to is the psychological stress some on this board seem to impose on themselves or others when their thinking becomes obsessive. Aged has found something that works well for him/her. Instead of applauding and encouraging the health he/she has found, you all dissect down to the smallest component and obsess over it. That's not the way to win people over, nor is it the way that the real world works. Any doctor would be overjoyed with Aged's results of 6.5% and would likely not change a thing, especially if the patient was content with the results. It doesn't always matter if better exists. There is such thing as good enough, which many of you won't learn on WebMD. It's why there are so many different treatment options. You pick the one that works best for each person, not the one that works best in a study or has the most potential for health. Compliance is so difficult to attain that it's considered a win to get to 6.5%, regardless of the path to get there. Many of you will hear me attacking Afrezza and being a "basher" or some other nonsense. I think Afrezza is the best insulin on the market and should be the go to meal-time insulin. It's sometimes difficult to read such strong opinions from people who have no experience outside of a textbook, medical journal, or website. Unfortunately, their arguments seem to pervade the rest of the board, leading to false expectations and just a general misunderstanding of how the real world works.                    |
|
|
|
Post by gareaudan on Jul 2, 2018 13:22:54 GMT -5
you are halving a relative number so you dont know if it is a small number or not. If at 6=2000 problems, then at 7=4000 and on that case, thats a lot. Your Graph dont show the absolut numbers si how can you say that its small? The gradient of the curve is what matters. If the gradient is small then the increase in risk is small and the incidence of complications will be virtually unchanged. That is the small number that matters. In theory a relative risk of 1 is the same risk as a non-diabetic person in 1996 when this data was collected, and since diabetic complications in that population are virtually nil then even doubling the risk represents a minimal increase in complications in real terms. ok i see what you mean. I didnt get at first that "relative risk of 1 is the same risk as a non-diabetic person". Thank for the explanation. I think that my point remain though. If we dont know the number of even at 6, we cannot really say anything. You said it is virtually nil but it cannot be zero otherwise any multiplier wouldnt make sense so what is virtually nil? If the study was made on 100 persons and that the number of event at 6 = 1 and at 7 = 2, it is different than an even at 6= 10 and at 7 = 20. In both case the gradient is the same (=2) but show very different results. Also, you said it is the gradient that matter but at the same Time that the value at 6 is too small to Said anything. The gradient between 6 and 7 is 2, no matter from where your starting. This is the point of having an relative scale no? |
|
|
|
Post by peppy on Jul 2, 2018 14:04:10 GMT -5
So the Stat Study/Affinity Poster. For subject-wise; 28/129 = 21.7% for TI 47/150 = 31.3% for Aspart (30.7% reduction in TI in number of subject experiencing severe HG events )
For number of event-wise; 59/129 = 0.457 per subject for TI 127/150 = 0.847 per subject for Aspart (46.0% reduction in TI in number of severe HG events per subject)
Among subjects with severe HG events; 59/28 = 2.1 events per subject for TI 127/47 = 2.7 events per subject for Aspart (22.0% reduction in TI in number of events per subject)
Conclusion: For TI less subject (30.7%) had severe HG event. If they do, TI subjects experience less frequently (22.0%). Overall, total number of severe HG events per subject is 46% less for TI.  The new advertising campaign? "Afrezza reduces your risk of severe hypoglycemia by 31%." (?) "Use of Afrezza significantly lowers the rate of hypoglycemia in Type 1 diabetes while providing similar or better glycemic control (54.1 events per subject vs. 78.2 events per subject, a reduction of 31%) On average, 26% lower rates of hypoglycemia were observed with Afrezza across the range of HbA1c levels, allowing the same degree of glycemic control with less hypoglycemia than insulin aspart."  |
|
|
|
Post by agedhippie on Jul 2, 2018 16:19:30 GMT -5
The gradient of the curve is what matters. If the gradient is small then the increase in risk is small and the incidence of complications will be virtually unchanged. That is the small number that matters. In theory a relative risk of 1 is the same risk as a non-diabetic person in 1996 when this data was collected, and since diabetic complications in that population are virtually nil then even doubling the risk represents a minimal increase in complications in real terms. ok i see what you mean. I didnt get at first that "relative risk of 1 is the same risk as a non-diabetic person". Thank for the explanation. I think that my point remain though. If we dont know the number of even at 6, we cannot really say anything. You said it is virtually nil but it cannot be zero otherwise any multiplier wouldnt make sense so what is virtually nil? If the study was made on 100 persons and that the number of event at 6 = 1 and at 7 = 2, it is different than an even at 6= 10 and at 7 = 20. In both case the gradient is the same (=2) but show very different results. Also, you said it is the gradient that matter but at the same Time that the value at 6 is too small to Said anything. The gradient between 6 and 7 is 2, no matter from where your starting. This is the point of having an relative scale no? Together with it's follow on, EDIC, the DCCT study is around 1,400 people (EDIC dropped to 1,300) over 30 years. DCCT is one of the core studies together with VADT, EDIC, and UKPDS that form the basis of diabetes complications data. That 1400 people were split into two groups, one with a target A1c of 6.05 (the intensive group), and the conventional group. After 10 years the mean A1c for the intensive group was a 7.2 and the conventional group was 9.1 and the active part of the project ended. EDIC was the continued tracking of the DCCT participants without intervention (they could do whatever they liked for control) and after another 16 - 20 years everyone's A1c settled around 8.0. Over 30 years 82 people had CVD events and 9 of those were fatal in the intensive group vs. 102 and 16 in the conventional group out that original 1,400. To reiterate - with an A1c of 7.2 rising to 7.8 there were 9 fatalities out of 711 people over 30 years, or 9 fatalities in 21,000 patient years. Looking at the conventional control arm with an A1c of 9.1 dropping to 8.2 (that's the effect of improved diabetes treatment) there were 16 fatalities out of 730 people over 30 years, or 16 fatalities in 21,000 patient years. The delta for intensive vs. regular control was 5 fatalities in 30 years. That can be expressed as a 55% increase in fatalities, but pretty meaningless in real terms. Anyway, there is your baseline - for an A1c of 7.5 expect about 9 additional fatalities over 30 years. This is the sort of reason I do not stress over my A1c that much. |
|
|
|
Post by gareaudan on Jul 2, 2018 16:31:46 GMT -5
ok i see what you mean. I didnt get at first that "relative risk of 1 is the same risk as a non-diabetic person". Thank for the explanation. I think that my point remain though. If we dont know the number of even at 6, we cannot really say anything. You said it is virtually nil but it cannot be zero otherwise any multiplier wouldnt make sense so what is virtually nil? If the study was made on 100 persons and that the number of event at 6 = 1 and at 7 = 2, it is different than an even at 6= 10 and at 7 = 20. In both case the gradient is the same (=2) but show very different results. Also, you said it is the gradient that matter but at the same Time that the value at 6 is too small to Said anything. The gradient between 6 and 7 is 2, no matter from where your starting. This is the point of having an relative scale no? Together with it's follow on, EDIC, the DCCT study is around 1,400 people (EDIC dropped to 1,300) over 30 years. DCCT is one of the core studies together with VADT, EDIC, and UKPDS that form the basis of diabetes complications data. That 1400 people were split into two groups, one with a target A1c of 6.05 (the intensive group), and the conventional group. After 10 years the mean A1c for the intensive group was a 7.2 and the conventional group was 9.1 and the active part of the project ended. EDIC was the continued tracking of the DCCT participants without intervention (they could do whatever they liked for control) and after another 16 - 20 years everyone's A1c settled around 8.0. Over 30 years 82 people had CVD events and 9 of those were fatal in the intensive group vs. 102 and 16 in the conventional group out that original 1,400. To reiterate - with an A1c of 7.2 rising to 7.8 there were 9 fatalities out of 711 people over 30 years, or 9 fatalities in 21,000 patient years. Looking at the conventional control arm with an A1c of 9.1 dropping to 8.2 (that's the effect of improved diabetes treatment) there were 16 fatalities out of 730 people over 30 years, or 16 fatalities in 21,000 patient years. The delta for intensive vs. regular control was 5 fatalities in 30 years. That can be expressed as a 55% increase in fatalities, but pretty meaningless in real terms. Anyway, there is your baseline - for an A1c of 7.5 expect about 9 additional fatalities over 30 years. This is the sort of reason I do not stress over my A1c that much. nice! Thanks for the numbers agedhippie, now i see what you mean. Appreciate it |
|
|
|
Post by sayhey24 on Jul 3, 2018 5:39:32 GMT -5
One thing I would be careful of is referencing old studies prior to CGM monitoring. I think what we will see is some studies showing the post meal spike is the greatest issue with heart disease. We need some good CGM based studies. In the mean time why take the chance. Take the afrezza, stop the spike its like a spike in the heart. STAT says nothing works like afrezza for post meal spikes.
|
|
|
|
Post by akemp3000 on Jul 3, 2018 7:06:37 GMT -5
Spot on sayhey. Using a CGM and stopping the spike "should" become the standard of care for most diabetics effective immediately. Dr. Kendall has the data to show that the current standard of care is not effective but Afrezza is. He obviously knows how the ADA works. This may take months but there's no reason this will take years regardless of past protocol. I would love to witness the ultimate debate with Dr. Kendall on one side and the big three pushing RAAs on the other. The ADA should schedule this debate immediately...ok, just wishing  BTW, preventing and stopping the mealtime spike should be Mannkind's marketing focus as it is the Afrezza advantage and exposes the weakness of competitors...and is something every diabetic understands. |
|
|
|
Post by akemp3000 on Jul 3, 2018 7:13:00 GMT -5
Here's a suggested marketing ad. Show how a CGM and Afrezza stops the spike using a video clip like this volleyball image then show volleyball defenders with horrible timing jumping up before and after the spike to imply how other options don't.
|
|
|
|
Post by agedhippie on Jul 3, 2018 8:13:48 GMT -5
One thing I would be careful of is referencing old studies prior to CGM monitoring. I think what we will see is some studies showing the post meal spike is the greatest issue with heart disease. We need some good CGM based studies. In the mean time why take the chance. Take the afrezza, stop the spike its like a spike in the heart. STAT says nothing works like afrezza for post meal spikes. On the contrary, DCCT/EDIC is a 30 year long study with 1,400 people. That is very solid data. The jury is still out on the significance of the meal time spike, at the moment it's taking the blame for a discrepancy in the CVD data where they cannot find the cause. However if it is going to make a difference the question is how much. Looking at the DCCT data which should be a worst case the answer is not a lot. Without trials the size of ACCORD at least this is all going to remain a theory. You have to prove the link and quantify the improvement. |
|
|
|
Post by agedhippie on Jul 3, 2018 8:21:06 GMT -5
Here's a suggested marketing ad. Show how a CGM and Afrezza stops the spike using a video clip like this volleyball image then show volleyball defenders with horrible timing jumping up before and after the spike to imply how other options don't. This is the traditional Afrezza marketing error. Undoubtedly Afrezza lowers the spike significantly, but what is the benefit and can it be proved? People here focus to much on features and not benefits. I don't care about the features, what is it going to do for me? Having a volleyball player who is strong, tall, and fast is of no use if they cannot get the ball over the net and into the right place. Their physical attributes are the features, using those features to get the ball where it is meant to be is the benefit and the only thing the audience cares about. |
|
|
|
Post by mango on Jul 3, 2018 8:27:25 GMT -5
One thing I would be careful of is referencing old studies prior to CGM monitoring. I think what we will see is some studies showing the post meal spike is the greatest issue with heart disease. We need some good CGM based studies. In the mean time why take the chance. Take the afrezza, stop the spike its like a spike in the heart. STAT says nothing works like afrezza for post meal spikes. Side note: Ca2+ homeostasis is regulated by CaMKII. When CaMKII becomes affected by hyperglycemia seen when there is loss of the FPIR, it leads to CaMKII inactivation in beta cells. There is probably global dysfunction in the signaling of calcium due to dysregulation in glucose homeostasis so this affects the heart leading to CaMKII inactivation & dysfunctioning in the heart > dysregulation in cardiac calcium homeostasis > cardiac dysfunction > cardiac disease processes. Restoring glucose homeostasis with Afrezza probably means restoring CaMKII functioning in the beta cells leading to restoration in circadian rhythm oscillations and clock gene expressions > restoring metabolic memory > restoring calcium homeostasis > prevention of cardiac disease processes.  |
|
|
|
Post by akemp3000 on Jul 3, 2018 8:31:45 GMT -5
According to Dr. Kendall, in a healthy body, BG peaks in about 45 minutes to an hour after a meal and leaves in about 2 hours. Afrezza mimics a healthy pancreas and also peaks in 45 minutes and departs in 2 hours. RAAs however peak in about 2 hours after a meal and leave in about 5 or 6 hours. Either Dr. Kendall is grossly misleading and wrong or this is very significant regarding meal time spikes and the relationship to the body. Diabetics know the significance of these meal time spikes. I'm going with Dr. Kendall and sayhey as their view appears to be based on current technology and science.
|
|
BTW, preventing and stopping the mealtime spike should be Mannkind's marketing focus as it is the Afrezza advantage and exposes the weakness of competitors...and is something every diabetic understands.