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Post by wsulylecoug on Jul 3, 2018 9:35:23 GMT -5
Questions from a non-diabetic who has gotten a crash course education in the last year or so since investing in MNKD...thanks to all here.
Is there an established or hypothesized threshold for the magnitude and duration of HbA1c swings (and cooresponding TIR) associated with reducing the suite of common long-term diabetic complications? This conversation seems to be focused on CVD. Is there an assumption that all other diabetic complications will react similarly to CVD? Nerve, kidney, eye, foot conditions etc?
Can similar HbA1c and TIR (one with Afrezza and one with RAA) improve long-term outcomes for one, two, maybe three complications, but not all, based solely on eliminating the length of time for uptake and exit (fast in fast out) benefit? All other numbers equal...does the in/out feature in and of itself create a long-term physical benefit for diabetics?
It would seem that providing an insulin most similar to what the body produces that functions most similar to how the body processes it would provide some benefit one way or another...that's a question and an uniformed statement.
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Post by peppy on Jul 3, 2018 9:51:26 GMT -5
Questions from a non-diabetic who has gotten a crash course education in the last year or so since investing in MNKD...thanks to all here. Is there an established or hypothesized threshold for the magnitude and duration of HbA1c swings (and cooresponding TIR) associated with reducing the suite of common long-term diabetic complications? This conversation seems to be focused on CVD. Is there an assumption that all other diabetic complications will react similarly to CVD? Nerve, kidney, eye, foot conditions etc?Can similar HbA1c and TIR (one with Afrezza and one with RAA) improve long-term outcomes for one, two, maybe three complications, but not all, based solely on eliminating the length of time for uptake and exit (fast in fast out) benefit? All other numbers equal...does the in/out feature in and of itself create a long-term physical benefit for diabetics? It would seem that providing an insulin most similar to what the body produces that functions most similar to how the body processes it would provide some benefit one way or another...that's a question and an uniformed statement. Talking type two here. Metabolic syndrome. My understanding is the glucose intolerance is one of first things to show up. Increased blood pressure. Hyperlipidemia and cardio vascular disease. Then you get the fatty liver. It turns out their is a limit to how much fat can be put in fat cells and the fat starts storing in our organs and muscle. I believe you asked if this could be reversed. There is a school of thought it can be reversed. I do not believe the American medical association saids it can be reversed.  |
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Post by mango on Jul 3, 2018 10:26:45 GMT -5
Postprandial hyperglycemia is associated with increased oxidative stress that results from development of AGEs, stimulation of the polyol pathway, and activation of protein kinase C. Elevated oxidative stress leads to and/or worsens impairment in endothelial function > atherosclerosis.
Oxidative stress associated with elevated PPG decreases levels of nitric oxide which leads to increased expression of nuclear factor-κB, resulting in elevated pro-inflammatory cytokines > atherosclerosis.
Elevated PPG and oxidative stress increase the risk of thrombosis via activation of platelets and increased thrombin generation. Excessively elevated PPG levels may elicit changes in the function of mesangial cells, pericytes, smooth muscle cells, and macrophages > increases risk of cardiovascular events.
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Post by agedhippie on Jul 3, 2018 13:46:12 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. Dr Kendall is wrong about the RAA timings and I have the CGM graphs to prove it  Humalog peaks after about an hour and clears in about 4 to 4.5 hours. Novolog and Apidra are faster. I think for the most part diabetics don't really care about meal time spikes unless they are in the 300s and even then they only care if they don't come back down. Science doesn't matter unless you can make people care about it, right now for the most part people don't care about meal time spikes. The people who do care are all on CGMs and eating restricted carb diets. |
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Post by sayhey24 on Jul 3, 2018 18:24:03 GMT -5
Aged - the problem is the insulin needs to peak at or right before the BG spike. 15 minutes later is just too late. Additionally, you need that robust release to signal the liver. Again, the RAAs are a dollar short and too little too late.
As far as "stopping the spike", I think if you follow the history of the CGM our understanding of TIR and spike stopping is just beginning. However, trying to argue that a PWD mimicking healthy pancreatic release is a bad thing sounds like a loser to me. Arguing the only ones who care about stopping the spike and they are already at 300 says they don't care or they would not be at 300. While we do all the studies to do another study, we already have the tools to stop the spike and keep the PWD 100% TIR at least while the PWD is awake.
Jardiance is touting heart healthy and why? Simple, lower overall BG levels. Yet, they are not stopping the spike. If they are getting the cardio results they are, think what afrezza does. Lower overall BG and no spikes sounds like a winner to me.
I think Dr. Kendall is correct when he said this is the easiest job he has ever had.
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Post by sayhey24 on Jul 3, 2018 18:52:50 GMT -5
Questions from a non-diabetic who has gotten a crash course education in the last year or so since investing in MNKD...thanks to all here. Is there an established or hypothesized threshold for the magnitude and duration of HbA1c swings (and cooresponding TIR) associated with reducing the suite of common long-term diabetic complications? This conversation seems to be focused on CVD. Is there an assumption that all other diabetic complications will react similarly to CVD? Nerve, kidney, eye, foot conditions etc? Can similar HbA1c and TIR (one with Afrezza and one with RAA) improve long-term outcomes for one, two, maybe three complications, but not all, based solely on eliminating the length of time for uptake and exit (fast in fast out) benefit? All other numbers equal...does the in/out feature in and of itself create a long-term physical benefit for diabetics? It would seem that providing an insulin most similar to what the body produces that functions most similar to how the body processes it would provide some benefit one way or another...that's a question and an uniformed statement. A1c and TIR are very different. When driving a car you have speedometer (TIR) an odometer (A1c) and a clock. If you drove 3 hours and the first hour drove 200 mph and the next 100mph and the next 60 mph what would your average mph(A1c) be? 360miles / 3 hours = 120. However during that hour at 200mph, your car was shaking and the bumper was falling off which is similar to the damage high BG levels will do to your cells.
Now you ask which cells? Which cells does your blood feed? Blood is a funny thing, it feeds all the cells and affects all the cells.
Now you ask "It would seem that providing an insulin most similar to what the body produces that functions most similar to how the body processes it would provide some benefit one way or another" That seems too easy and common sense but is 100% correct. The problem is until afrezza this was not possible. If afrezza was developed 121 years ago their would be no antigycemics today nor the RAAs. The problem is we have a $25+billion established market and the companies making those other drugs have a lot to loose and they will do pretty much anything not to.
Additionally, "insulin" has a really bad name in the diabetes space. No T2 wants to take insulin. Insulin is dangerous, requires needles, is a big mess and if you are on insulin you are near the end. While afrezza is none of these people know this amino acid powder as insulin and associate it with the old school insulins. Right now MNKD has a huge marketing hurdle.
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Post by uvula on Jul 3, 2018 19:19:15 GMT -5
You folks are going in circles. I hope we don't drive the old hippie away from the message boards. We desperately need his reality based perspective.
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Post by goyocafe on Jul 3, 2018 19:52:56 GMT -5
You folks are going in circles. I hope we don't drive the old hippie away from the message boards. We desperately need his reality based perspective. Agreed, but it feels all too often that he’s pissing on my campfire.🤠 |
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Post by agedhippie on Jul 3, 2018 20:08:36 GMT -5
Aged - the problem is the insulin needs to peak at or right before the BG spike. 15 minutes later is just too late. Additionally, you need that robust release to signal the liver. Again, the RAAs are a dollar short and too little too late. As far as "stopping the spike", I think if you follow the history of the CGM our understanding of TIR and spike stopping is just beginning. However, trying to argue that a PWD mimicking healthy pancreatic release is a bad thing sounds like a loser to me. Arguing the only ones who care about stopping the spike and they are already at 300 says they don't care or they would not be at 300. While we do all the studies to do another study, we already have the tools to stop the spike and keep the PWD 100% TIR at least while the PWD is awake. Jardiance is touting heart healthy and why? Simple, lower overall BG levels. Yet, they are not stopping the spike. If they are getting the cardio results they are, think what afrezza does. Lower overall BG and no spikes sounds like a winner to me. I think Dr. Kendall is correct when he said this is the easiest job he has ever had. You are entirely correct in that there is a lack of data around TIR and Standard Deviation (the spike). This is an area that desperately needs studying. However without that trial data nothing is going to change because there is nothing to support the change. Jardiance gives improved CVD results after adjustment for the A1c reduction so it's not the lower A1c that causes it (actually the A1c reduction is mediocre). I have yet to see an explanation for why it happens but it certainly seems to work. |
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Post by agedhippie on Jul 3, 2018 20:10:22 GMT -5
You folks are going in circles. I hope we don't drive the old hippie away from the message boards. We desperately need his reality based perspective. Agreed, but it feels all too often that he’s pissing on my campfire.🤠 Sorry, that's a side effect of the magic mushrooms, they are a diuretic.  |
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Post by goyocafe on Jul 3, 2018 20:13:51 GMT -5
Agreed, but it feels all too often that he’s pissing on my campfire.🤠 Sorry, that's a side effect of the magic mushrooms, they are a diuretic. So long as you don’t come home with “ Dragon Slayer” tattooed on your back, you’re good. 🐉 |
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Post by peppy on Jul 3, 2018 20:36:30 GMT -5
Aged - the problem is the insulin needs to peak at or right before the BG spike. 15 minutes later is just too late. Additionally, you need that robust release to signal the liver. Again, the RAAs are a dollar short and too little too late. As far as "stopping the spike", I think if you follow the history of the CGM our understanding of TIR and spike stopping is just beginning. However, trying to argue that a PWD mimicking healthy pancreatic release is a bad thing sounds like a loser to me. Arguing the only ones who care about stopping the spike and they are already at 300 says they don't care or they would not be at 300. While we do all the studies to do another study, we already have the tools to stop the spike and keep the PWD 100% TIR at least while the PWD is awake. Jardiance is touting heart healthy and why? Simple, lower overall BG levels. Yet, they are not stopping the spike. If they are getting the cardio results they are, think what afrezza does. Lower overall BG and no spikes sounds like a winner to me. I think Dr. Kendall is correct when he said this is the easiest job he has ever had. You are entirely correct in that there is a lack of data around TIR and Standard Deviation (the spike). This is an area that desperately needs studying. However without that trial data nothing is going to change because there is nothing to support the change. Jardiance gives improved CVD results after adjustment for the A1c reduction so it's not the lower A1c that causes it (actually the A1c reduction is mediocre). I have yet to see an explanation for why it happens but it certainly seems to work.
In many of the postmarketing reports, and particularly in patients with type 1 diabetes, the presence of ketoacidosis was not immediately recognized and institution of treatment was delayed because presenting blood glucose levels were below those typically expected for diabetic ketoacidosis (often less than 250 mg/dL). Signs and symptoms at presentation were consistent with dehydration and severe metabolic acidosis and included nausea, vomiting, abdominal pain, generalized malaise, and shortness of breath. In some but not all cases, factors predisposing to ketoacidosis such as insulin dose reduction, acute febrile illness, reduced caloric intake due to illness or surgery, pancreatic disorders suggesting insulin deficiency (e.g., type 1 diabetes, history of pancreatitis or pancreatic surgery), and alcohol abuse were identified. Before initiating JARDIANCE, consider factors in the patient history that may predispose to ketoacidosis including pancreatic insulin deficiency from any cause, caloric restriction, and alcohol abuse. In patients treated with JARDIANCE consider monitoring for ketoacidosis and temporarily discontinuing JARDIANCE in clinical situations known to predispose to ketoacidosis (e.g., prolonged fasting due to acute illness or surgery). 5.3 Acute Kidney Injury and Impairment in Renal Function JARDIANCE causes intravascular volume contraction [see Warnings and Precautions (5.1)] and can cause renal impairment [see Adverse Reactions (6.1)]. There have been postmarketing reports of acute kidney injury, some requiring hospitalization and dialysis, in patients receiving SGLT2 inhibitors, including JARDIANCE; some reports involved patients younger than 65 years of age.Before initiating JARDIANCE, consider factors that may predispose patients to acute kidney injury including hypovolemia, chronic renal insufficiency, congestive heart failure and concomitant medications (diuretics, ACE inhibitors, ARBs, NSAIDs). Consider temporarily discontinuing JARDIANCE in any setting of reduced oral intake (such as acute illness or fasting) or fluid losses (such as gastrointestinal illness or excessive heat exposure); monitor patients for signs and symptoms of acute kidney injury. If acute kidney injury occurs, discontinue JARDIANCE promptly and institute treatment. JARDIANCE increases serum creatinine and decreases eGFR. Patients with hypovolemia may be more susceptible to these changes. Renal function abnormalities can occur after initiating JARDIANCE [see Adverse Reactions (6.1)]. Renal function should be evaluated prior to initiation of JARDIANCE and monitored periodically thereafter. More frequent renal function monitoring is recommended in patients with an eGFR below 60 mL/min/1.73 m2. Use of JARDIANCE is not recommended when eGFR is persistently less than 45 5.4 Urosepsis and Pyelonephritis There have been postmarketing reports of serious urinary tract infections including urosepsis and pyelonephritis requiring hospitalization in patients receiving SGLT2 inhibitors, including JARDIANCE. Treatment with SGLT2 inhibitors increases the risk for urinary tract infections. Evaluate patients for signs and symptoms of urinary tract infections and treat promptly, if indicated [see Adverse Reactions (6)]. 5.5 Hypoglycemia with Concomitant Use with Insulin and Insulin Secretagogues Insulin and insulin secretagogues are known to cause hypoglycemia. The risk of hypoglycemia is increased when JARDIANCE is used in combination with insulin secretagogues (e.g., sulfonylurea) or insulin [see Adverse Reactions (6.1)]. Therefore, a lower dose of the insulin secretagogue or insulin may be required to reduce the risk of hypoglycemia when used in combination with JARDIANCE. docs.boehringer-ingelheim.com/Prescribing%20Information/PIs/Jardiance/jardiance.pdfVolume Depletion JARDIANCE causes an osmotic diuresis, which may lead to intravascular volume contraction and adverse reactions related to volume depletion. In the pool of five placebo-controlled clinical trials, adverse reactions related to volume depletion (e.g., blood pressure (ambulatory) decreased, blood pressure systolic decreased, dehydration, hypotension, hypovolemia, orthostatic hypotension, and syncope) were reported by 0.3%, 0.5%,and 0.3% of patients treated with placebo, JARDIANCE 10 mg, and JARDIANCE 25 mg, respectively. JARDIANCE may increase the risk of hypotension in patients at risk for volume contraction [see Warnings and Precautions (5.1) and Use in Specific Populations (8.5, 8.6)]. * What the heck-o-li kind of placebo pill reduces blood/plasma volume? Hmmmm
Increased Urination In the pool of five placebo-controlled clinical trials, adverse reactions of increased urination (e.g., polyuria, pollakiuria, and nocturia) occurred more frequently on JARDIANCE than on placebo (see Table 1). Specifically, nocturia was reported by 0.4%, 0.3%, and 0.8% of patients treated with placebo, JARDIANCE 10 mg, and JARDIANCE 25 mg, respectively. In a long-term cardiovascular outcome trial, the acute impairment in renal function was observed to reverse after treatment discontinuation suggesting acute hemodynamic changes play a role in the renal function changes observed with empagliflozin. |
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Post by sophie on Jul 3, 2018 22:28:06 GMT -5
Is there an established or hypothesized threshold for the magnitude and duration of HbA1c swings (and cooresponding TIR) associated with reducing the suite of common long-term diabetic complications? This conversation seems to be focused on CVD. Is there an assumption that all other diabetic complications will react similarly to CVD? Nerve, kidney, eye, foot conditions etc? Can similar HbA1c and TIR (one with Afrezza and one with RAA) improve long-term outcomes for one, two, maybe three complications, but not all, based solely on eliminating the length of time for uptake and exit (fast in fast out) benefit? All other numbers equal...does the in/out feature in and of itself create a long-term physical benefit for diabetics? It would seem that providing an insulin most similar to what the body produces that functions most similar to how the body processes it would provide some benefit one way or another...that's a question and an uniformed statement. As far as I'm aware, the exact mechanism hasn't been proven. Diabetes exerts its effects on all vessels in the body, but it's the small vessels that get noticed first. There is a theory that damage is done to the vessels by AGEs- advanced glycation end products, which are essentially reduced sugars paired with amino acids or lipids. These molecules are fairly stable and can coalesce, blocking bloodflow through small vessels, leading to ischemia and eventual death of nerve and tissue distal to those vessels. This sets off an inflammatory response that is normally handled by cells in your body called macrophages, which try to oxidize the molecules to enzymatically break them apart and chew them up. However, once these macrophages get overwhelmed, they turn into what are called foam cells, and will later calcify and harden, which damages the vessels even more. To answer your question, adding the correct amount of insulin at the proper time will decrease the amount of glucose and lipids in the bloodstream at any given time. Physiologically speaking, the body is supposed to store glucose- usually into triglycerides- when insulin is secreted, turning on the "fed" state. This should also "turn off" lipoprotein lipase, the enzyme responsible for breaking apart triglycerides into free fatty acids that later combine with glucose to form AGEs. So, in effect, insulin kills two birds with one stone when used properly. This is true in all vessels, so fewer glucose & lipid molecules in the blood means that organs are getting better oxygenation and perfusion, ie. no ischemia and death. The other benefit of fast in/fast out is that insulin is a hormone. You don't want to keep the "fed" state always turned on. The "fasting" state needs to do its work also, otherwise your heart and other organs would balloon in size from all the newly stored fat. It is good to have some lipids and glucose in the blood, but just enough, as these are energy molecules used by the cells in your body to function. So it's a balancing act. Too much or too little is a bad thing. This is what makes Afrezza so useful and unique. You want insulin to remove enough glucose from the blood to provide energy for cells, but not too much that you end up storing unnecessary amounts of glucose as fat. From the studies I have read, when used properly, Afrezza would both lower end organ damage and keep you weight neutral as long as you're eating a reasonable diet. This is a two-pronged decrease in mortality risk as obesity carries with it it's own slew of problems. |
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Post by mnkdfann on Jul 3, 2018 23:41:02 GMT -5
You are entirely correct in that there is a lack of data around TIR and Standard Deviation (the spike). This is an area that desperately needs studying. However without that trial data nothing is going to change because there is nothing to support the change. Jardiance gives improved CVD results after adjustment for the A1c reduction so it's not the lower A1c that causes it (actually the A1c reduction is mediocre). I have yet to see an explanation for why it happens but it certainly seems to work.
In many of the postmarketing reports, and particularly in patients with type 1 diabetes, the presence of ketoacidosis was not immediately recognized and institution of treatment was delayed because presenting blood glucose levels were below those typically expected for diabetic ketoacidosis (often less than 250 mg/dL). Signs and symptoms at presentation were consistent with dehydration and severe metabolic acidosis and included nausea, vomiting, abdominal pain, generalized malaise, and shortness of breath. In some but not all cases, factors predisposing to ketoacidosis such as insulin dose reduction, acute febrile illness, reduced caloric intake due to illness or surgery, pancreatic disorders suggesting insulin deficiency (e.g., type 1 diabetes, history of pancreatitis or pancreatic surgery), and alcohol abuse were identified. Before initiating JARDIANCE, consider factors in the patient history that may predispose to ketoacidosis including pancreatic insulin deficiency from any cause, caloric restriction, and alcohol abuse. In patients treated with JARDIANCE consider monitoring for ketoacidosis and temporarily discontinuing JARDIANCE in clinical situations known to predispose to ketoacidosis (e.g., prolonged fasting due to acute illness or surgery). 5.3 Acute Kidney Injury and Impairment in Renal Function JARDIANCE causes intravascular volume contraction [see Warnings and Precautions (5.1)] and can cause renal impairment [see Adverse Reactions (6.1)]. There have been postmarketing reports of acute kidney injury, some requiring hospitalization and dialysis, in patients receiving SGLT2 inhibitors, including JARDIANCE; some reports involved patients younger than 65 years of age.Before initiating JARDIANCE, consider factors that may predispose patients to acute kidney injury including hypovolemia, chronic renal insufficiency, congestive heart failure and concomitant medications (diuretics, ACE inhibitors, ARBs, NSAIDs). Consider temporarily discontinuing JARDIANCE in any setting of reduced oral intake (such as acute illness or fasting) or fluid losses (such as gastrointestinal illness or excessive heat exposure); monitor patients for signs and symptoms of acute kidney injury. If acute kidney injury occurs, discontinue JARDIANCE promptly and institute treatment. JARDIANCE increases serum creatinine and decreases eGFR. Patients with hypovolemia may be more susceptible to these changes. Renal function abnormalities can occur after initiating JARDIANCE [see Adverse Reactions (6.1)]. Renal function should be evaluated prior to initiation of JARDIANCE and monitored periodically thereafter. More frequent renal function monitoring is recommended in patients with an eGFR below 60 mL/min/1.73 m2. Use of JARDIANCE is not recommended when eGFR is persistently less than 45 5.4 Urosepsis and Pyelonephritis There have been postmarketing reports of serious urinary tract infections including urosepsis and pyelonephritis requiring hospitalization in patients receiving SGLT2 inhibitors, including JARDIANCE. Treatment with SGLT2 inhibitors increases the risk for urinary tract infections. Evaluate patients for signs and symptoms of urinary tract infections and treat promptly, if indicated [see Adverse Reactions (6)]. 5.5 Hypoglycemia with Concomitant Use with Insulin and Insulin Secretagogues Insulin and insulin secretagogues are known to cause hypoglycemia. The risk of hypoglycemia is increased when JARDIANCE is used in combination with insulin secretagogues (e.g., sulfonylurea) or insulin [see Adverse Reactions (6.1)]. Therefore, a lower dose of the insulin secretagogue or insulin may be required to reduce the risk of hypoglycemia when used in combination with JARDIANCE. docs.boehringer-ingelheim.com/Prescribing%20Information/PIs/Jardiance/jardiance.pdfVolume Depletion JARDIANCE causes an osmotic diuresis, which may lead to intravascular volume contraction and adverse reactions related to volume depletion. In the pool of five placebo-controlled clinical trials, adverse reactions related to volume depletion (e.g., blood pressure (ambulatory) decreased, blood pressure systolic decreased, dehydration, hypotension, hypovolemia, orthostatic hypotension, and syncope) were reported by 0.3%, 0.5%,and 0.3% of patients treated with placebo, JARDIANCE 10 mg, and JARDIANCE 25 mg, respectively. JARDIANCE may increase the risk of hypotension in patients at risk for volume contraction [see Warnings and Precautions (5.1) and Use in Specific Populations (8.5, 8.6)]. * What the heck-o-li kind of placebo pill reduces blood/plasma volume? Hmmmm
Increased Urination In the pool of five placebo-controlled clinical trials, adverse reactions of increased urination (e.g., polyuria, pollakiuria, and nocturia) occurred more frequently on JARDIANCE than on placebo (see Table 1). Specifically, nocturia was reported by 0.4%, 0.3%, and 0.8% of patients treated with placebo, JARDIANCE 10 mg, and JARDIANCE 25 mg, respectively. In a long-term cardiovascular outcome trial, the acute impairment in renal function was observed to reverse after treatment discontinuation suggesting acute hemodynamic changes play a role in the renal function changes observed with empagliflozin. Are you intentionally throwing shade at the god known as David Kendall? Jardiance was his baby. www.reuters.com/article/usa-healthcare-diabetes/exclusive-us-insurers-hold-back-lillys-death-defying-diabetes-drug-idUSL1N1211PP20151002David Kendall, vice president of medical affairs for Lilly’s diabetes franchise, said he hopes insurers will allow greater use of Jardiance as soon as possible, and that medical societies will promptly update their treatment guidelines to prescribe Jardiance instead of other treatments. “We would hope undue delay isn’t an outcome; we would hope for timely decision-making,” Kendall said. www.drugdeliverybusiness.com/boehringer-ingelheims-jardiace-cuts-risk-cardiovascular-death-t2d-patients/“Cardiovascular disease is the primary cause of death in people with Type II diabetes,” Dr. David Kendall, Lilly Diabetes’ distinguished medical fellow, said. “The results presented at EASD provide further evidence of the benefit empagliflozin can provide to patients with different background blood sugar control.” |
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Post by wsulylecoug on Jul 5, 2018 9:42:58 GMT -5
Thanks for the responses. Did some more reading on the net about the suite of side effects and it sounds like most everything is tied to adverse changes in blood vessels big and small at some level.
On a side note, for the past couple of weeks, I've been working for a Type I diabetic who had been assisting me with some light physical labor. He's in his 70's and it was obvious his blood sugars were off now and then. At one point he was down to 80 and chugged a big glass of juice. He is on a pump and bolus's with injections. I had to ask if he had heard of Afrezza and he had. He thought it was only approved for Type II, so I told him it was approved for both. Gave him a very short run down on the speed of action and some of the general outcomes of the STAT study. His response was that he saw the longer tail of the injection as a benefit to deal with residual sugars. His injection is based on carb counting. He had an appointment with his endo the following day in Wenatchee WA...we both live in Ellensburg WA. It turns out the am and pm had been reversed on his pump so his blood sugars had been off for the last several months and was feeling better. He didn't mention anything more about Afrezza and I didn't push it because he seemed satisfied with where he was at. While he appeared impressed with the improvements that came with the use of Afrezza, it didn't seem to be enough to make a change...for now. Maybe sometime down the road, but the feeling I got was that his control was good enough with his current treatment methods to continue whats he's doing.
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