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Post by sayhey24 on Oct 6, 2024 7:12:29 GMT -5
Would you like to address the reason why if a PWD takes afrezza prior to spiking and they stop the spike which let say would spike to 200 they may need 25% of the afrezza than what they need after they spike? Now, you are saying the body is making more insulin than it needs, yet if afrezza stops the spike we need a lot less afrezza and a lot less of all the insulin the body is releasing. Why is that? Why does the body become more resistant to insulin after the body has been releasing its insulin? You would think since the body has already released all that insulin, it has a jump start on afrezza and you would need less afrezza? Nope, you need more and usually a lot more. ... This is the last time I am answering this question for you since it has been answered several times already so you don't appear to be retaining the information. As your blood sugar rises you become more insulin resistant. This occurs in T1 and T2 giving a lower I:C ratio so you need more insulin. If you stop the spike then your I:C ratio isn't changing so you don't need that 25% more insulin. The body definitely gets the jump on Afrezza,with it's own insulin, but the body cannot produce enough insulin to overcome the insulin resistance and so you have a relative deficiency. Adding insulin, any insulin, fills that gap. however, it makes matters worse as you down regulate the insulin receptors even harder, but you can always add more insulin - there is no upper limit. Insulin is a brute force approach which is why it's not popular with doctors who would rather address the issue with drugs that improve insulin sensitivity where they can. This is all 101 stuff and any diabetes textbook will explain it for you, you just need to read. Some endos prescribe GLP-1 for T1, not for weight loss but rather to increase insulin sensitivity. That's off-label though. OK - so before you told me the body is making insulin and maybe to much insulin. Now its not making enough. I would also say we are saying different things. With afrezza, its actually replacing first phase release and getting to the cells before the body's insulin. The thing is if the body's insulin gets there first is when you become resistant and we need more, a lot more afrezza. Since afrezza can mimic 1st phase release the body is not as you say getting a jump on afrezza. The idea with afrezza is to get a jump on the body's insulin before you incur the resistance. Most textbooks do not including afrezza. Since some T1s are still producing some insulin. The endos prescribing GLP1s for those people might makes sense. Then again they would be better prescribing afrezza and stopping the spike. |
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Post by sayhey24 on Oct 6, 2024 7:24:21 GMT -5
I get a little confused when I hear of the concept of Beta Cells resting. I get that they’re overloaded when a person over eats, and eventually worked to failure, but I think of it like Testosterone. Your balls shrink when you take steroids (not that I would know, never done it, going on what I’ve heard) because they are resting, as you’re replacing what they would normally produce. After repeated abuse many can’t produce Testosterone on their own any more and for some Testosterone replacement becomes for life. Wouldn’t that be the same with insulin and Beta Cells? What they can see through autopsy with T2s are 3 groupings of beta cells; clumps which are dead; healthy cells; and shriveled cells which are still doing something. Prior to covid there was not much belief that diabetes was viral based. With covid there are more in that camp however its probably not in the textbooks. Lets say for argument sake it is and the cells are infected. What you would want is for them to rest and work less and hope the immune system can have a positive impact before the infection spreads which it seems to do as more and more insulin is released. What we do know through a zillion studies is early insulin intervention has shown to stop progression. What Al Mann saw with afrezza was reversal which he saw as a cure for some PWDs. This is why he put $B of his own money into this. |
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Post by agedhippie on Oct 6, 2024 8:06:50 GMT -5
OK - so before you told me the body is making insulin and maybe to much insulin. Now its not making enough. I would also say we are saying different things. You are just trolling now. Of course your body can make extra insulin, it doesn't mean it can make enough extra insulin for it's increased needs. |
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Post by peppy on Oct 6, 2024 9:45:39 GMT -5
I get a little confused when I hear of the concept of Beta Cells resting. I get that they’re overloaded when a person over eats, and eventually worked to failure, but I think of it like Testosterone. Your balls shrink when you take steroids (not that I would know, never done it, going on what I’ve heard) because they are resting, as you’re replacing what they would normally produce. After repeated abuse many can’t produce Testosterone on their own any more and for some Testosterone replacement becomes for life. Wouldn’t that be the same with insulin and Beta Cells? This caught my attention. Testosterone has my attention. Also making testosterone levels go down are Phthalates, which get into the androgen receptors, once in the androgen receptors the feed back system thinks there is enough testosterone. Phthalate-induced testosterone/androgen receptor pathway disorder on spermatogenesis and antagonism of lycopene pubmed.ncbi.nlm.nih.gov/36104915/weehaw,  .https://www.sciencedirect.com/science/article/abs/pii/S1532045622002332 ars.els-cdn.com/content/image/1-s2.0-S1532045622002332-ga1_lrg.jpg |
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Post by agedhippie on Oct 6, 2024 10:19:28 GMT -5
What they can see through autopsy with T2s are 3 groupings of beta cells; clumps which are dead; healthy cells; and shriveled cells which are still doing something. ... What we do know through a zillion studies is early insulin intervention has shown to stop progression. What Al Mann saw with afrezza was reversal which he saw as a cure for some PWDs. This is why he put $B of his own money into this. I think you will find in an autopsy all the beta cells are dead, or the police are going to want a word! I can find about a dozen studies so I think zillions is a stretch. However, this looks like a really easy trial to do, although the timeline is long. The existing trials all follow the same pattern, treat newly diagnosed Type 2 diabetics with around two weeks of insulin to reestablish normal levels and then stop. The results are fairly consistent with around a 50% failure rate at the one year mark. How hard would it be for MNKD to get 150 candidates and give them Afrezza for two weeks and then check in every few months? Best of all it's an open timeline as with UKDPS - you can see how long remission persists. |
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Post by prcgorman2 on Oct 7, 2024 7:16:49 GMT -5
What they can see through autopsy with T2s are 3 groupings of beta cells; clumps which are dead; healthy cells; and shriveled cells which are still doing something. ... What we do know through a zillion studies is early insulin intervention has shown to stop progression. What Al Mann saw with afrezza was reversal which he saw as a cure for some PWDs. This is why he put $B of his own money into this. I think you will find in an autopsy all the beta cells are dead, or the police are going to want a word! I can find about a dozen studies so I think zillions is a stretch. However, this looks like a really easy trial to do, although the timeline is long. The existing trials all follow the same pattern, treat newly diagnosed Type 2 diabetics with around two weeks of insulin to reestablish normal levels and then stop. The results are fairly consistent with around a 50% failure rate at the one year mark. How hard would it be for MNKD to get 150 candidates and give them Afrezza for two weeks and then check in every few months? Best of all it's an open timeline as with UKDPS - you can see how long remission persists. I wonder if variations on that theme might discover a “treat to succeed” protocol? Is it possible through diet, exercise, and Multiple Daily Inhalations (MDI)  to “heal” the pancreas where remission is effectively permanent? How successful? 20% of those on the regime? 80%? None? |
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Post by agedhippie on Oct 7, 2024 8:28:26 GMT -5
I wonder if variations on that theme might discover a “treat to succeed” protocol? Is it possible through diet, exercise, and Multiple Daily Inhalations (MDI) to “heal” the pancreas where remission is effectively permanent? How successful? 20% of those on the regime? 80%? None? You cannot heal the pancreas (that it the holy grail) but you can reduce the load to the point where you can live within the limits it can handle. The issue is that Type 2 is heterogeneous and progressive, there are a lot of variants and some are more aggressive than others. If you have an aggressive form you are not going to outrun it, but for a milder variant you may well be able to make remission permanent. This is why treat to fail exists, in some case there will be no failure, but in others failure can follow within months. The kicker is that you don't know which variation you are dealing with until the treatment fails so doctors treat for the best case and increment as needed. |
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to “heal” the pancreas where remission is effectively permanent? How successful? 20% of those on the regime? 80%? None?