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Post by sportsrancho on Mar 11, 2023 19:10:55 GMT -5
I know I noticed it was pretty old and there was a place you can click for updates so I did and it said there weren’t any at this time.
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Post by agedhippie on Mar 11, 2023 21:52:54 GMT -5
I know I noticed it was pretty old and there was a place you can click for updates so I did and it said there weren’t any at this time. i believe that's corrections to the article usually rather than updates to the topic itself.
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Post by sayhey24 on Mar 12, 2023 7:35:58 GMT -5
What did Al Mann tell us? The medically correct way to treat the T2 diabetic is to treat the "post prandial glucose excursions". As I told Stevil I don't make this up. You can argue Al Mann was wrong but I would say don't go there. TIR is needed with T1s because of the sleeping hours and how things can go sideways. T2s don't have that issue. TIR is a T1 thing. I am not going to "Get Doctors" and neither is Mike nor MNKD. Robert Ford is on a mission to sell CGMs to the T2 market. He needs to get T2s on insulin ASAP. He could careless what insulin. That is counter to the SoC. I will happily say that Al Mann was wrong since it's theory and not fact. There is no data to support this. If you think T2 diabetics do not have night time issues you have obviously never heard of dawn phenomenon. You will find the 62% number on Mannkind's web site (actually 62.5%.) I would certainly hope Robert Ford wants to sell CGMs. However, the target is $10B over the next 5 years (so 2028) as discussed that at the J.P. Morgan Healthcare Conference. That's 15% CAGR which given a global product is an easy reach. The $25B number by 2025 for Libre is fantasy. And the elephant in the room. There is no way Abbott direct their sales people to defraud Medicare which is what you are proposing. That's even assuming you could get the prescription past the insurer given that a lot of coverage requires prior approval or step therapy. This idea is a flight of fantasy, but by all means invest based on it. At this point I think we are arguing in circles; I go by the data and you go by faith in your ideas. Those cannot be reconciled so I am going to drop this. Going back to the point of this thread - the risk of SBO with GLP-1. Just like amyloid deposits this is so rare that nobody cares, it does make a good headline though (Daily Mail - you do know their reputation don't you?). The clear benefits outweigh the risk and that's how medicine works. OK - for some reason I think I must have hit a sore spot. You seem to really be shaken the CMS is now providing CGM payment for "insulin treated" seniors. For Robert Ford to gets those words in the policy was a surprise but a very pleasant surprise. Lets get something straight - Abbott and not me was behind the CMS CGM payment changes and the words "insulin treated". You have gone as far as to say I am suggesting that the Abbott reps doing their job and convincing doctors to prescribe insulin sooner and maybe much sooner than the SoC "guidelines" suggest is FRAUD! Wow, that is a bridge too far for me. You say you are all about facts yet you want to make up your own. Now you are saying that the Medicare insurance provider is going to reject insulin treatment for a patient after the doctor has prescribed it after they agreed in their bid to CMS to provide it. That one we will have to watch. I think thats a made up fantasy on your part. We have know forever early insulin treatment has huge benefits but now its FRAUD! You are also challenging the way the human body works and say its theory and not fact. As Gary Scheiner says "Think like a Pancreas". How does the pancreas work? What does it do during fasting and mealtimes? Can we mimic that? If we can then that's the approach we want to take. I am glad Robert gave himself another 3 years to 2028. 2025 seemed way to aggressive for me to go from $4B to $10B - thats a lot of new insulin and maybe afrezza scripts. It will also allow for Mike to get his afrezza T2 plan together. And the topper - the Daily Mail is not a reputable news source and I will add neither is the NY Post but lets believe everything in the NY Times and WaPo - come on man!!!
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Post by sayhey24 on Mar 12, 2023 7:46:14 GMT -5
Welcome to being a doctor 😁. These are considerations I make with each patient. There are never any absolutes in medicine. It is all risk/benefit analysis. We’re playing the same waiting game with Afrezza, at least all of us but say hey. Medicine will never advance if we’re too afraid to take the first step. The only way we now know afrezza is *probably* safe is because we can look backwards and see that it is. We’ll do the same with GLP-1s. Sometimes we get it wrong. When that happens, you adjust. It’s why the first step for me when I treat diabetes is to address the underlying cause first. I stress diet and exercise changes, because THAT is the safest and best first line treatment for diabetes. Then we go from there… Stevil - what is the underlying cause of T2 diabetes? What have autopsies of the pancreas of obese non-diabetic people shown us? How about recent Covid T2 diabetics?
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Post by agedhippie on Mar 12, 2023 10:16:26 GMT -5
Welcome to being a doctor 😁. These are considerations I make with each patient. There are never any absolutes in medicine. It is all risk/benefit analysis. We’re playing the same waiting game with Afrezza, at least all of us but say hey. Medicine will never advance if we’re too afraid to take the first step. The only way we now know afrezza is *probably* safe is because we can look backwards and see that it is. We’ll do the same with GLP-1s. Sometimes we get it wrong. When that happens, you adjust. It’s why the first step for me when I treat diabetes is to address the underlying cause first. I stress diet and exercise changes, because THAT is the safest and best first line treatment for diabetes. Then we go from there… Stevil - what is the underlying cause of T2 diabetes? What have autopsies of the pancreas of obese non-diabetic people shown us? How about recent Covid T2 diabetics? There is probably a Nobel prize waiting for the person who can answer that question. The problem is that Type 2 is a classification (antibody negative diabetes) rather than a single disease so there are a lot of variants.
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Post by agedhippie on Mar 12, 2023 10:42:00 GMT -5
OK - for some reason I think I must have hit a sore spot. You seem to really be shaken the CMS is now providing CGM payment for "insulin treated" seniors. For Robert Ford to gets those words in the policy was a surprise but a very pleasant surprise. Funny, I was thinking the same thing. Remember this? You could be right but first they have to get Medicare approval. Do you think Merck, Nova Nordisk, Lilly and the rest want T2s using a CGM showing PPG excursions without the cover of a mealtime insulin??? They think they are getting approval by July and the NICE study is what they are banking on but this is the only study I see and its for T1s. www.nice.org.uk/guidance/ng17/evidence/b-continuous-glucose-monitoring-in-adults-with-type-1-diabetes-pdf-11013435182.
I was right. I told you it would get approved. Remember this? You ask how long will the doctor keep prescribing the CGM? As long as he keeps prescribing afrezza and that's as long as the rep keeps coming with that big lunch buffet and other goodies.
Sorry, but that is fraud and there is no way that Abbott would countenance that approach. The really stupid thing about the idea is the conclusion that this CMS change allows Afrezza users to get CGMs where they couldn't before. Afrezza counts as MDI and as such you can already get a CGM from Medicare if you use Afrezza. And yet somehow we don't have reps proposing defrauding Medicare (" Neither the GP nor the Abbott rep really care if the PWD ever uses afrezza") to doctors currently. Anyway, if you want to believe Abbott will do have at it! I have explained why it's silly and you are free to ignore it. The truth is that we will see from the Afrezza prescription sales if you are right.
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Post by stevil on Mar 12, 2023 12:05:12 GMT -5
@sayhey I’ll be honest with you. I’m not really motivated to get into arguments with you as you have shown you are set in your ways, don’t accept evidence that contradicts your narrowed and constrained focus and beliefs. It’s an exercise in futility and I don’t have the time, energy, nor determination to see it through. Here is a podcast I listened to recently, from someone who researches diabetes and is aware of the latest theories. While I don’t hold Joplin in the same esteem as you, he does mention them and gives them good remarks. I remember awhile back you stating insulin resistance wasn’t a thing and there being an issue with the junk the pancreas secretes. Both of those are… interesting… comments, neither of which make sense or have evidence to back them up. In any case, please accept my resignation on this matter. I wanted to address your question, but as I stated above, I don’t want to keep dedicating more time and energy to this. My children would like to see their father 😁. I don’t think I’ve disagreed with anything aged has said, so if you need more to chew on, your conversations with him may serve as a primer… as well as proof that you have been presented plenty of dissenting information but have apparently chosen to disregard it because you refuse to accept that you’re wrong. Here is the link to the podcast. I hope it will be of benefit to you. podcasts.apple.com/us/podcast/the-peter-attia-drive/id1400828889?i=1000586933595
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Post by sayhey24 on Mar 12, 2023 18:39:45 GMT -5
@sayhey I’ll be honest with you. I’m not really motivated to get into arguments with you as you have shown you are set in your ways, don’t accept evidence that contradicts your narrowed and constrained focus and beliefs. It’s an exercise in futility and I don’t have the time, energy, nor determination to see it through. Here is a podcast I listened to recently, from someone who researches diabetes and is aware of the latest theories. While I don’t hold Joplin in the same esteem as you, he does mention them and gives them good remarks. I remember awhile back you stating insulin resistance wasn’t a thing and there being an issue with the junk the pancreas secretes. Both of those are… interesting… comments, neither of which make sense or have evidence to back them up. In any case, please accept my resignation on this matter. I wanted to address your question, but as I stated above, I don’t want to keep dedicating more time and energy to this. My children would like to see their father 😁. I don’t think I’ve disagreed with anything aged has said, so if you need more to chew on, your conversations with him may serve as a primer… as well as proof that you have been presented plenty of dissenting information but have apparently chosen to disregard it because you refuse to accept that you’re wrong. Here is the link to the podcast. I hope it will be of benefit to you. podcasts.apple.com/us/podcast/the-peter-attia-drive/id1400828889?i=1000586933595Stevil - we can show there is "insulin resistance" but there is a difference between insulin resistance "existing" and being the "root cause". My contention is it is a symptom. Shulman's assumption and I am Assuming yours is its the root cause. Why are we now seeing all these T2s after getting covid when we can show covid has attacked the pancreas and beta cells? You may be too young to remember but the "accepted truth" for the cause of ulcers use to be acid food. At the time this could not be questioned kind of like insulin resistance is the cause of T2s. I will probably reach out to Shulman and have him try this experiment but you can do it too. Try this as a simple experiment - have the T2 eat but stop the spike - how much afrezza do you need? Have the same person eat and spike and then try to bring down the BG - how much afrezza do you need? Its the same amount of carbohydrates so you would think you would need the same amount of afrezza not 2x or 3x. What has changed??? Why is that you need so much more? Is that insulin resistance? It seems to be but why does it change in such as short time? Doctor Shulman is assuming insulin resistance is the cause and what I am demonstrating is its a changing symptom. Then he takes the next step and attributes cancer to insulin resistance when he is really meaning out of control blood sugar. Then they ask us to take a "leap of faith" in the discussion and I will pass. I will stick with Richard Bernstein on this and say you need to keep tight glucose control. Also what happens with insulin resistance when tight glucose control is maintained in the T2? I will say at one point he does talk about beta cells not making enough insulin and reversing insulin resistance by significantly reducing calorie intake. Why are they able to do this he mentions the toxic lipid"? Then he says the problem is with the transport mechanism - I will buy this. Then they throw up their hands and say "we don't know" - great. I just got to say this guy did not impress me. I am glad you are agreeing so much with Aged. He needs some good support as he seems be losing it a bit as he does not like the fact that CMS is now paying for CGMs with "insulin treated" senior. I was not aware you had kids. Take my life advance I gave you in a previous post with the kids as they grow older in finding out what they are doing.
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Post by sayhey24 on Mar 12, 2023 19:04:09 GMT -5
OK - for some reason I think I must have hit a sore spot. You seem to really be shaken the CMS is now providing CGM payment for "insulin treated" seniors. For Robert Ford to gets those words in the policy was a surprise but a very pleasant surprise. Funny, I was thinking the same thing. Remember this? You could be right but first they have to get Medicare approval. Do you think Merck, Nova Nordisk, Lilly and the rest want T2s using a CGM showing PPG excursions without the cover of a mealtime insulin??? They think they are getting approval by July and the NICE study is what they are banking on but this is the only study I see and its for T1s. www.nice.org.uk/guidance/ng17/evidence/b-continuous-glucose-monitoring-in-adults-with-type-1-diabetes-pdf-11013435182.
I was right. I told you it would get approved. Remember this? You ask how long will the doctor keep prescribing the CGM? As long as he keeps prescribing afrezza and that's as long as the rep keeps coming with that big lunch buffet and other goodies.
Sorry, but that is fraud and there is no way that Abbott would countenance that approach. The really stupid thing about the idea is the conclusion that this CMS change allows Afrezza users to get CGMs where they couldn't before. Afrezza counts as MDI and as such you can already get a CGM from Medicare if you use Afrezza. And yet somehow we don't have reps proposing defrauding Medicare (" Neither the GP nor the Abbott rep really care if the PWD ever uses afrezza") to doctors currently. Anyway, if you want to believe Abbott will do have at it! I have explained why it's silly and you are free to ignore it. The truth is that we will see from the Afrezza prescription sales if you are right. Aged - Today the SoC says for the T2 they get basal first and then you have to wait for MDI. The problem Robert Ford has is how many T2s are on MDI - afrezza or not? If they are they, already have the CGM but that market is very small. This is not about MDI. Abbott wants the entire 20M medicare T2s. They want those metformin users jumping to insulin usage, today not in two years. I do believe Abbott will jump the SoC and have insulin prescribed before step 4. I know Robert Ford wants insulin prescribed ASAP so he can sell CGMs. Assuming afrezza makes the formularity in 2024 afrezza only has to be prescribed for "corrections". It does not need to be MDI. If the CGM shows the BG spiking take the afrezza. If not don't bother. Is this the ideal way to use afrezza - NO but it will sell CGMs. So now you are saying doctors getting a lunch buffet and listening to the sales reps advice is fraud. Wow - how long have we known early insulin intervention has significant benefits. I bet Robert Ford has a study or two showing this. Its anything but fraud. Would it be to the PWDs benefit to properly use the afrezza - absolutely. Does the Abbott sales rep care if they do? Their job is selling the CGM and if afrezza gets the job done great. While I understand this is really bothering you it is by no means fraud. Its called selling a product and getting the rules changed to help do so. I think they call that lobbying.
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Post by stevil on Mar 16, 2023 11:27:51 GMT -5
@sayhey I’ll be honest with you. I’m not really motivated to get into arguments with you as you have shown you are set in your ways, don’t accept evidence that contradicts your narrowed and constrained focus and beliefs. It’s an exercise in futility and I don’t have the time, energy, nor determination to see it through. Here is a podcast I listened to recently, from someone who researches diabetes and is aware of the latest theories. While I don’t hold Joplin in the same esteem as you, he does mention them and gives them good remarks. I remember awhile back you stating insulin resistance wasn’t a thing and there being an issue with the junk the pancreas secretes. Both of those are… interesting… comments, neither of which make sense or have evidence to back them up. In any case, please accept my resignation on this matter. I wanted to address your question, but as I stated above, I don’t want to keep dedicating more time and energy to this. My children would like to see their father 😁. I don’t think I’ve disagreed with anything aged has said, so if you need more to chew on, your conversations with him may serve as a primer… as well as proof that you have been presented plenty of dissenting information but have apparently chosen to disregard it because you refuse to accept that you’re wrong. Here is the link to the podcast. I hope it will be of benefit to you. podcasts.apple.com/us/podcast/the-peter-attia-drive/id1400828889?i=1000586933595Stevil - we can show there is "insulin resistance" but there is a difference between insulin resistance "existing" and being the "root cause". My contention is it is a symptom. Shulman's assumption and I am Assuming yours is its the root cause. Why are we now seeing all these T2s after getting covid when we can show covid has attacked the pancreas and beta cells? You may be too young to remember but the "accepted truth" for the cause of ulcers use to be acid food. At the time this could not be questioned kind of like insulin resistance is the cause of T2s. I will probably reach out to Shulman and have him try this experiment but you can do it too. Try this as a simple experiment - have the T2 eat but stop the spike - how much afrezza do you need? Have the same person eat and spike and then try to bring down the BG - how much afrezza do you need? Its the same amount of carbohydrates so you would think you would need the same amount of afrezza not 2x or 3x. What has changed??? Why is that you need so much more? Is that insulin resistance? It seems to be but why does it change in such as short time? Doctor Shulman is assuming insulin resistance is the cause and what I am demonstrating is its a changing symptom. Then he takes the next step and attributes cancer to insulin resistance when he is really meaning out of control blood sugar. Then they ask us to take a "leap of faith" in the discussion and I will pass. I will stick with Richard Bernstein on this and say you need to keep tight glucose control. Also what happens with insulin resistance when tight glucose control is maintained in the T2? I will say at one point he does talk about beta cells not making enough insulin and reversing insulin resistance by significantly reducing calorie intake. Why are they able to do this he mentions the toxic lipid"? Then he says the problem is with the transport mechanism - I will buy this. Then they throw up their hands and say "we don't know" - great. I just got to say this guy did not impress me. I am glad you are agreeing so much with Aged. He needs some good support as he seems be losing it a bit as he does not like the fact that CMS is now paying for CGMs with "insulin treated" senior. I was not aware you had kids. Take my life advance I gave you in a previous post with the kids as they grow older in finding out what they are doing. It's all there. Just need to listen to the podcast podcasts.apple.com/us/podcast/the-peter-attia-drive/id1400828889?i=1000586933595It's a very compelling argument. He will take you step by step down the biochemical pathway, discuss NMR results, show you trial data. It all supports insulin resistance as the root cause of not only diabetes, but most metabolic disease. I'm honestly not sure why you're so fixated on Covid/viruses as the root cause of diabetes. How do you explain diabetes before covid? Why is diabetes fully correlative with the obesity epidemic? As a species, we have had viruses throughout history. Why, all of the sudden, as we have gotten fatter, are we starting to develop diabetes at a much higher rate than ever before? I'm not necessarily discounting that viruses may cause diabetes. There are probably hundreds of mechanisms. But, by far, the most predominant form is from insulin resistance. Again, I have no interest in continuing to debate you over this. Listen to the podcast. If you don't come away convinced, I don't know what to tell you. In my opinion, it's iron tight as a theory.
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Post by sayhey24 on Mar 16, 2023 15:24:27 GMT -5
Stevil - we can show there is "insulin resistance" but there is a difference between insulin resistance "existing" and being the "root cause". My contention is it is a symptom. Shulman's assumption and I am Assuming yours is its the root cause. Why are we now seeing all these T2s after getting covid when we can show covid has attacked the pancreas and beta cells? You may be too young to remember but the "accepted truth" for the cause of ulcers use to be acid food. At the time this could not be questioned kind of like insulin resistance is the cause of T2s. I will probably reach out to Shulman and have him try this experiment but you can do it too. Try this as a simple experiment - have the T2 eat but stop the spike - how much afrezza do you need? Have the same person eat and spike and then try to bring down the BG - how much afrezza do you need? Its the same amount of carbohydrates so you would think you would need the same amount of afrezza not 2x or 3x. What has changed??? Why is that you need so much more? Is that insulin resistance? It seems to be but why does it change in such as short time? Doctor Shulman is assuming insulin resistance is the cause and what I am demonstrating is its a changing symptom. Then he takes the next step and attributes cancer to insulin resistance when he is really meaning out of control blood sugar. Then they ask us to take a "leap of faith" in the discussion and I will pass. I will stick with Richard Bernstein on this and say you need to keep tight glucose control. Also what happens with insulin resistance when tight glucose control is maintained in the T2? I will say at one point he does talk about beta cells not making enough insulin and reversing insulin resistance by significantly reducing calorie intake. Why are they able to do this he mentions the toxic lipid"? Then he says the problem is with the transport mechanism - I will buy this. Then they throw up their hands and say "we don't know" - great. I just got to say this guy did not impress me. I am glad you are agreeing so much with Aged. He needs some good support as he seems be losing it a bit as he does not like the fact that CMS is now paying for CGMs with "insulin treated" senior. I was not aware you had kids. Take my life advance I gave you in a previous post with the kids as they grow older in finding out what they are doing. It's all there. Just need to listen to the podcast podcasts.apple.com/us/podcast/the-peter-attia-drive/id1400828889?i=1000586933595It's a very compelling argument. He will take you step by step down the biochemical pathway, discuss NMR results, show you trial data. It all supports insulin resistance as the root cause of not only diabetes, but most metabolic disease. I'm honestly not sure why you're so fixated on Covid/viruses as the root cause of diabetes. How do you explain diabetes before covid? Why is diabetes fully correlative with the obesity epidemic? As a species, we have had viruses throughout history. Why, all of the sudden, as we have gotten fatter, are we starting to develop diabetes at a much higher rate than ever before? I'm not necessarily discounting that viruses may cause diabetes. There are probably hundreds of mechanisms. But, by far, the most predominant form is from insulin resistance. Again, I have no interest in continuing to debate you over this. Listen to the podcast. If you don't come away convinced, I don't know what to tell you. In my opinion, it's iron tight as a theory. Stevil - The SARS-CoV-2 virus is just one of the viruses attacking the beta cells. I don't think that is up for debate. We see it in autopsies and lab experiments. We also know there are a lot more people getting T2 after having Covid. That is also a fact. Joslin isolated 4 other distinct viruses years ago and were working on more. God only knows what the total virus population could be. One theory is we have T2 hotspots because the virus has spread in a community like Pottsville PA. Is that theory correct IDK but Pottsville is not like the Puma indians which we can dismiss to being a gene thing. What happens if different viruses attack the beta cells? I bet you would have variants of diabetes. We also know from autopsy that fat non-diabetics grow more beta cells. The body adapts. Thats a fact based on autopsy. Blaming diabetes on gaining too much weight does not work with a healthy body. It is only after the beta cells have been compromised and can no longer grow enough mass to make "good" insulin. It is also not what the tech diet companies are seeing. They are seeing loss of post prandial control prior to the weight gain. Based on what you are saying it should be the other way around. I did reach out the Gerry Shulman and poised the same question to him which I did to you. Why is it that insulin resistance can rapidly increase when we do not stop the post meal spike? When I hear back I will let you know what his answer is. Did you try the post meal spike experiment with afrezza? I bet if you did you see what I am saying.
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Post by agedhippie on Mar 16, 2023 18:22:20 GMT -5
Stevil - The SARS-CoV-2 virus is just one of the viruses attacking the beta cells. I don't think that is up for debate. We see it in autopsies and lab experiments. We also know there are a lot more people getting T2 after having Covid. That is also a fact. Joslin isolated 4 other distinct viruses years ago and were working on more. God only knows what the total virus population could be. One theory is we have T2 hotspots because the virus has spread in a community like Pottsville PA. Is that theory correct IDK but Pottsville is not like the Puma indians which we can dismiss to being a gene thing. What happens if different viruses attack the beta cells? I bet you would have variants of diabetes. We also know from autopsy that fat non-diabetics grow more beta cells. The body adapts. Thats a fact based on autopsy. Blaming diabetes on gaining too much weight does not work with a healthy body. It is only after the beta cells have been compromised and can no longer grow enough mass to make "good" insulin. It is also not what the tech diet companies are seeing. They are seeing loss of post prandial control prior to the weight gain. Based on what you are saying it should be the other way around. I did reach out the Gerry Shulman and poised the same question to him which I did to you. Why is it that insulin resistance can rapidly increase when we do not stop the post meal spike? When I hear back I will let you know what his answer is. Did you try the post meal spike experiment with afrezza? I bet if you did you see what I am saying. That theory was discredited by Mount Sinai researchers last year. They found that COVID attacks all of the pancreas, not just the beta cells, and additionally the cells did not die. The evidence that COVID caused diabetes is not now generally thought to be reliable. As to Type 2 diabetes the current view is that this a combination of people who were previously diabetic but undiagnosed (CDC reckons about 8.5 million people in the US are undiagnosed) who were uncovered either in treatment or follow-up, and people who became diabetic for a period under the stress from the disease (high cortisol levels will do that) but cleared up afterwards. It's likely that the latter group are predisposed towards diabetes (think pre-diabetic) and would have developed diabetes anyway. With weight you are conflating issues. Weight causes insulin resistance which the body reacts to by building extra beta cells. Certain genes compromise the build out of those beta cells and hence you get diabetes. This is why diet and exercise helps with diabetes because it reduces your insulin resistance to a point where your insulin is sufficient again (the Newcastle Diet). Lacking the relevant genes you can grow to the size of a small killer whale with no sign of diabetes. It's interesting that you pick Joslin because they have done a lot of works into genetics and epigenetics relating to Type 2. I expect his admin either deletes it before it even gets to him, or sends a rote response (after all you may want to donate money). Either way until there is trial data showing a link nobody will be interested because it's just another random theory, although they may fake it for a decent sized donation
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Post by sayhey24 on Mar 16, 2023 19:15:22 GMT -5
Stevil - The SARS-CoV-2 virus is just one of the viruses attacking the beta cells. I don't think that is up for debate. We see it in autopsies and lab experiments. We also know there are a lot more people getting T2 after having Covid. That is also a fact. Joslin isolated 4 other distinct viruses years ago and were working on more. God only knows what the total virus population could be. One theory is we have T2 hotspots because the virus has spread in a community like Pottsville PA. Is that theory correct IDK but Pottsville is not like the Puma indians which we can dismiss to being a gene thing. What happens if different viruses attack the beta cells? I bet you would have variants of diabetes. We also know from autopsy that fat non-diabetics grow more beta cells. The body adapts. Thats a fact based on autopsy. Blaming diabetes on gaining too much weight does not work with a healthy body. It is only after the beta cells have been compromised and can no longer grow enough mass to make "good" insulin. It is also not what the tech diet companies are seeing. They are seeing loss of post prandial control prior to the weight gain. Based on what you are saying it should be the other way around. I did reach out the Gerry Shulman and poised the same question to him which I did to you. Why is it that insulin resistance can rapidly increase when we do not stop the post meal spike? When I hear back I will let you know what his answer is. Did you try the post meal spike experiment with afrezza? I bet if you did you see what I am saying. That theory was discredited by Mount Sinai researchers last year. They found that COVID attacks all of the pancreas, not just the beta cells, and additionally the cells did not die. The evidence that COVID caused diabetes is not now generally thought to be reliable. As to Type 2 diabetes the current view is that this a combination of people who were previously diabetic but undiagnosed (CDC reckons about 8.5 million people in the US are undiagnosed) who were uncovered either in treatment or follow-up, and people who became diabetic for a period under the stress from the disease (high cortisol levels will do that) but cleared up afterwards. It's likely that the latter group are predisposed towards diabetes (think pre-diabetic) and would have developed diabetes anyway. With weight you are conflating issues. Weight causes insulin resistance which the body reacts to by building extra beta cells. Certain genes compromise the build out of those beta cells and hence you get diabetes. This is why diet and exercise helps with diabetes because it reduces your insulin resistance to a point where your insulin is sufficient again (the Newcastle Diet). Lacking the relevant genes you can grow to the size of a small killer whale with no sign of diabetes. It's interesting that you pick Joslin because they have done a lot of works into genetics and epigenetics relating to Type 2. I expect his admin either deletes it before it even gets to him, or sends a rote response (after all you may want to donate money). Either way until there is trial data showing a link nobody will be interested because it's just another random theory, although they may fake it for a decent sized donation Aged - I have seen the autopsy reports on Covid. We see good cells, shriveled cells and dead cells. They don't all die. I would be more than glad to review what Mount Sinai "discredited" if you can provide the link and tell me who funded their study. Was it published in the NY Times - Ha! Maybe this is what you are talking about? They are not saying it does not infect the beta cells they are saying its worse. It infects all the pancreatic cells including the beta cells. They are also saying the infected cells generally did not die as a result - which is correct. Some are OK and some die and some get shriveled up and are still trying to release something which I call "bad insulin". Then again I am a simple guy. I am sure there is a much more complicated term. As Dr. Homman says send me more money "a history of SARS-CoV-2 infection may yet promote prolonged glycometabolic perturbations and even an increase in cumulative diabetes risk in vulnerable populations. Over the next few years, we need to pay careful attention to emerging observational and retrospective studies" or as I would simply put - send me more money! You got to love that term glycometabolic perturbations - man that is good. Its got to be worth $500k in study funds.www.mountsinai.org/about/newsroom/2022/sars-cov-two-infection-likely-not-associated-with-increased-risk-of-new-onset-diabetesWhat you are saying about weight causing the resistance is not what it being seen with CGM results. The reason diet and exercise works is first the pancreas needs to release less "insulin" as the reduce body mass is "taking the load" off the pancreas and the insulin need is reduced. Exercise helps because of the same reason TZDs help - you make new cells (muscle with exercise vs fat) with brand new receptors. The reason non-diabetic obese grow additional beta cells is because of the increased body mass and the body's need for additional insulin. The diabetic obese don't grow the additional beta cell mass. I did not pick Joslin. Al Mann pointed me to it. Al worked very closely with Joslin when first developing his pumps and I think thats where Gary Scheiner became one of the first users of Al's pumps. Aged - I will ask you the same question regarding insulin resistance since you think Gerry Shulman won't answer. Why is it if you stop the spike the T2 needs 2x maybe 3x less than if they spike and then try and bring down the spike with the same carb load? Why does the insulin resistance change so rapidly? Its clearly not a theory as we can demonstrate it.
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Post by agedhippie on Mar 16, 2023 23:22:17 GMT -5
... What you are saying about weight causing the resistance is not what it being seen with CGM results. The reason diet and exercise works is first the pancreas needs to release less "insulin" as the reduce body mass is "taking the load" off the pancreas and the insulin need is reduced. Exercise helps because of the same reason TZDs help - you make new cells (muscle with exercise vs fat) with brand new receptors. The reason non-diabetic obese grow additional beta cells is because of the increased body mass and the body's need for additional insulin. The diabetic obese don't grow the additional beta cell mass. ... Aged - I will ask you the same question regarding insulin resistance since you think Gerry Shulman won't answer. Why is it if you stop the spike the T2 needs 2x maybe 3x less than if they spike and then try and bring down the spike with the same carb load? Why does the insulin resistance change so rapidly? Its clearly not a theory as we can demonstrate it. I might not have phrased that clearly enough in my post. Restating; the loss of weight reduces the insulin resistance which means your beta cells can now produce enough insulin to maintain your levels. (There is still the issue of this not working over time since diabetes is progressive, but in the immedate and ideally medium term this is true.) Exercise reduces levels in the long term because of weight loss, and in the short term because fast-twitch muscles take up glucose directly (no insulin involved) from the blood stream. And diabetic obese people do grow additional mass, just not as much as they need. The answer is simple, as your blood glucose increases so does your insulin resistance as your receptors down regulate. Terminating the spike early avoids down regulation but does not solve insulin resistance - this is why dosing is not always a simple ratio. If you want to understand about insulin resistance properly I suggest this paper, Trends in insulin resistance: insights into mechanisms and therapeutic strategy, which explains the multiple mechanism for insulin resistance and signaling.
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Post by sayhey24 on Mar 19, 2023 7:12:55 GMT -5
Wow - now you are trying to blame rising blood glucose as the cause for resistance.
I thought we have already shown through autopsy that the body will adapt to rising blood glucose by growing more beta cells. Thats what happens and its demonstrable. We also know there is 1st phase release and second phase and the healthy pancreas will keep pumping out insulin until the BG is brought back to baseline. If you have a healthy pancreas you don't get the insulin resistance.
What you are suggesting is insulin resistance comes first but yet its caused by high blood sugar. So whats causing the resistance if we know the healthy pancreas is made to deal with it and even grows more beta cells? You see you can't have it both ways. Its a circular argument. The healthy body is built to handle the need for extra insulin capacity even as we get fat.
This is a beauty from your paper - "Accumulation of reports have demonstrated that IR is a complex metabolic disorder with integrated pathophysiology. The exact causes of IR has not been fully determined". I thought I had posted several Covid related papers demonstrating its impacts on beta cells.
One thing I have come to the conclusion on is this discussion is ending up like the discussion I have had over the last three years that Covid came from an undercooked batburger with a side of pangolin fries. Some people really want to believe that. Yesterday I even heard it was not from the batburger but from a raccoon dog in the wet market. I am not buying that either.
I think the one thing we can agree on is if we stop the rising blood glucose in its tracks - "Stop the Spike" then we can reduce the resistance - so lets focus on that. Your batburger theory says IR will be reduced by lowing high glucose. I can demonstrate that by "Stopping the Spike" we need 2x 3x less insulin to get the PWD back to baseline.
Now the question is - Can we do that with basal or metformin or SGLT2 or GLP1? Can we agree the answer is NO? Can we agree that RAAs are better but are still too damn slow? Can we agree the only thing that can "Stop the Spike" is a healthy pancreas or afrezza? If the answer is yes and we know the answer is yea, lets focus on how afrezza can change T2 diabetic care instead of spending time rearguing batburger theories.
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