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Post by peppy on Jun 8, 2022 17:19:33 GMT -5
Great discussion/debate. "If the diagnosis is insulin deficiency, the solution is insulin" One of the main issues seems to be whether insulin deficiency is a symptom or a diagnosis. Insulin deficiency doesn't develop until later in the disease, which is why beta cell exhaustion is the predominant theory. No one really knows the real cause for sure, at least not when I was in medical school and I haven't heard any updates since. During the early stages of type 2, serum insulin levels increase, presumably because muscle/fat/liver become resistant to insulin binding at its receptor. (theoretically) This results in the body telling the pancreas to secrete more insulin since it isn't receiving the normal feedback mechanism that insulin has done what it was supposed to do. Beyond what I have already shared, further evidence exists that would lend support to the insulin resistance theory. There have been insulin receptors identified on muscle, fat, liver, and brain tissue- GLUT receptors- that are believed to either have conformational change (meaning the receptor either changes size/shape so that insulin fits/doesn't fit) or the receptors get up/down regulated depending on the body's needs. The implications of this is that it takes resources to maintain a receptor and if it is no longer needed, it can be recycled for use elsewhere, or it is binding insulin that isn't needed. In layman's terms, GLUT receptors are the insulin binding receptors on muscle/fat/brain/liver etc. In times of high energy need, more insulin receptors are needed because glucose=energy. When energy is not needed, the receptors are no longer needed and the body doesn't want to keep the receptors active when glycogen stores are full, so the receptors either change shape or are eliminated to reduce the uptake of additional energy. It has been proven that exercise will restore this functionality of the receptors since more energy is needed to take up glucose, once again pointing to a metabolic component to the disease. Keep in mind, the GLUT receptors are not the only cells that become resistant to insulin, but they are the predominant ones. You can literally flip them on or off with being sedentary or active. A virus would not behave that way. Having said all that, the question remains, what is the best way to treat a chronic disease? Is insulin the answer? Previous insulins have caused an increase in cardiovascular disease (one of the biggest and worst causes of mortality from the disease) while GLP-1s have shown to decrease cardiovascular disease and many other long-term complications. There has never been an insulin that does its job and then leaves when the job is done, so it's hard to say whether the resulting complications from insulin therapy are the result of long-acting insulin and if this effect would be ameliorated by Afrezza's speed and efficiency. Diabetes is not solely a glucose and insulin problem. There are many other metabolic pathways affected in the disease. Manipulation of which pathway produces the best results? We don't know yet. Insulin has been tried and failed with pretty poor results, but it was different than Afrezza. We don't have too much long term data on GLP-1s yet, but they appear to have fairly promising results with long-term use when judging by the resultant complications of the disease outside of A1c control. We may find that a combination of treatment is ideal with a multi-pronged approach of mixing the two together. Whatever the answer is, it is not a simple one and there is not yet enough information available to definitively answer the question. , I was in on everything you said, I learn from you. Here is my catch 22, Manipulation of which pathway produces the best results? We don't know yet. Insulin has been tried and failed with pretty poor results, but it was different than Afrezza. Have we fooled ourselves to believe we are the pathway manipulators and we know how to do it? I am nervous to have my pathway manipulated. How about you? Pathway manipulation that works barometric surgery. Just sayin. |
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Post by sayhey24 on Jun 8, 2022 18:50:46 GMT -5
To add to my previous post a point I didn't fully communicate. pubmed.ncbi.nlm.nih.gov/28958751/Our bodies are wonderfully made and are complicated beyond belief. It seems that any imbalance causes problems in the system, even providing an excess of what is considered "good". The reason we need new trials with Afrezza is that a lot of damage done by insulin may be mitigated by the rapidity of Afrezza's speed. We know, with certainty, that an excess of insulin causes worsening disease. However, if insulin finishes its job and doesn't hang around afterwards, would that provide better results? We won't know until we do more studies... Are GLP-1s safe by the same logic? We won't know until time tells the tale. As of now, it appears they are profoundly safe. Millions are on the medications and are getting positive results. Time will reveal the negative issues, if any, that come from manipulating glucagon analogues. Good grief Stevil! Go back and read the original study your link is based on and we can then discuss why the base study was not properly done. I think Jenny Ruhl has a nice summary on why that study is bogus. If someone thinks keeping a PWD below 140 which is the goal with afrezza and near normal BG levels is going to cause increased heart attacks then all the non PWDs have big issues. What we do know is a BG for long periods of time case vascular damage and that leads to heart attacks and the #1 cause of death in PWDs are heart attacks. |
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Post by sayhey24 on Jun 8, 2022 20:30:26 GMT -5
Insulin is a growth hormone. To answer your question, I don’t know that Afrezza is weight neutral. Not much data has been published. Possible reasons why could be less inflammation, insulin doesn’t hang around as long so less fat production, less metabolic effect. Regardless, more data and study is needed. mounjaro is hijacking a metabolic mechanism to trick the body into not storing fat and to actually release fat stores in the body. Insulin can actually drive glucose into fat and increase production… I’ll flip your insulin resistance question back onto you to shed light on why I don’t buy a common etiology between the two diseases. Why is it that you could give a type 2 diabetic 100 units of lantus a day and still not achieve proper basal control, while that same dose would be lethal to probably any single type 1 that exists? The reason is that the issue isn’t solely with insulin production but an actual disruption to the body’s ability to use insulin. The reason an obese person would have hypertrophic beta cells is they likely don’t have the gene that codes for a weaker beta cell and are able to properly compensate. The current prevailing theory is beta cell exhaustion for type 2 and I fins that to be far more plausible than an antibody mediated response to a virus. I do believe type 1s could be viral. But if type 1s modify their lifestyle with diet and exercise, if they have bariatric surgery, if they start early intensive insulin treatment for beta cell rest, there is little to no change to their disease and they still become fully insulin dependent once all beta cells are lost. A viral etiology makes no sense in a reversible disease that does not target antibodies. As I stated before, insulin resistance does not appear to cause diabetes necessarily. There appears to be another component. But it nearly always predates the loss of beta cell function. I would expect the beta cell loss first if viral. there are also a myriad of other metabolic issues that are linked to diabetes. Obesity, hypertension, hyperlipidemia, fatty liver. Why would other metabolic conditions increase diabetes I viral? I suppose you could take the immunocompromised angle, but a metabolic cause seems to be far more consistent. i keep forgetting to add one of the most compelling pieces to the argument against a viral etiology- gestational diabetes. How can a woman go in and out of diabetes (sometimes multiple times) and not later go on to develop the disease after child birth if a virus causes the disease? Why would gestational diabetes increase the risk of later developing the disease if purely viral? Again, I feel a metabolic cause is the far more likely answer. Stevil - you say "Insulin is a growth hormone" There was actually some lengthy discussion on this at the Adcom as one of the "experts" was arguing insulin to be a growth hormone and afrezza would promote tumor development in the lung. Of course that never materialized. Actually insulin is a peptide hormone with a high degree of homology with the insulin-like growth factor I (IGF-I) but its not IGF-I. Not only that you have a ton of insulin floating around in your body everyday. The idea with afrezza is to provide that same level your body was making before the beta cells got messed up. you say "I don’t know that Afrezza is weight neutral" afrezza is human insulin, nothing more. Its going to do what human insulin does. Insulin neither causes weight nor reduces weight. Caloric intake does that. However, the general belief is subq insulin cases weight gain which is not really the case. What happens is those taking subq insulin tend to snack more to balance their BG levels and with high BG the body is not converting the food you eat into energy. This lack of energy causes an increase in hunger so people eat more. However - if you look at the Affinity1 trial you will see "there was also a significant difference in weight outcomes. Patients in the AFREZZA-Gen2 group lost an average of 0.39 kg over the treatment period compared to an average gain of 0.93 kg in the insulin aspart group (p=0.0102)" Why -well they didn't use CGMs with the trial so we don't have AGPs but my guess is the post meal spike with afrezza was blunted reducing the hunger urge and with reduced hypos they were drinking less orange juice. investors.mannkindcorp.com/news-releases/news-release-details/mannkind-reports-positive-data-phase-3-clinical-study-afrezzayou say - "I’ll flip your insulin resistance question back onto you" OK, the father of metformin is also the principle creator of the insulin resistance theory. Ralph's funding is from non-insulin research. If the simple answer was they just need to take insulin, thats not good for funding. However, if the story is the body is making enough insulin, insulin is not the issue then metformin, GLP1s, etc make more sense and more research funding from BP. you say - "Why is it that you could give a type 2 diabetic 100 units of lantus a day" Well, unless you know this T2 I sure would not start there. However the viral theory is that in addition to destroying the beta cells the virus is affecting the released insulin creating "bad" insulin which is attaching to the cell receptors and blocking them or what the smart people call "impaired insulin clearance". This was first reported in 1949 so its nothing new by Broh-Kahn RH, Mirsky IA. The inactivation of insulin by tissue extracts; the effect of fasting on the insulinase content of rat liver. So the story goes whatever these viruses are doing to the beta cells the released insulin makes a mess at the receptor. If your T2 has blocked up receptors your 100 units is able to get to new cells or unblock some of the blocked one. We also know its not one virus and now with covid we have more evidence and there will be a lot more research. Why the viral research was dropped years ago is a "mystery" but with covid there is renewed interest and evidence. At least one good thing came from covid and its not my $5 a gallon gas. you say - "i keep forgetting to add one of the most compelling pieces to the argument against a viral etiology- gestational diabetes. How can a woman go in and out of diabetes (sometimes multiple times) and not later go on to develop the disease after child birth if a virus causes the disease" The beta cells are not producing enough insulin for the pregnant women's needs. We typically have no AGPs prior to her getting pregnant. What was her post prandial glucose like before. Is she some how picking up the virus after becoming pregnant and her immune system is acting different? As we have seen with covid viral load changes and fluctuate and one day you have less and another day more. The bottom line is we need a head to head trial against Mounjaro for A1C. I don't care about weight in this trial I only care about A1C. If Mounjaro is really good at having people lose weight great. After we start the T2s on afrezza and dial in their dosage we can add Mounjaro to give them a bellyache so they have no appetite. I bet the more they feel nauseated the less they will eat and the more weight they will lose. If we get them a health coach maybe like a Nutrisense maybe they can even lose more. |
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Post by stevil on Jun 8, 2022 21:03:19 GMT -5
I don't think we're getting anywhere as we're both seemingly firmly entrenched in our own sides. I think we may just have to agree to disagree.
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Post by prcgorman2 on Jun 9, 2022 0:36:12 GMT -5
Short cuts make long delays. - Peregrin Took (JRR Tolkien)
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Post by sayhey24 on Jun 9, 2022 5:38:49 GMT -5
I don't think we're getting anywhere as we're both seemingly firmly entrenched in our own sides. I think we may just have to agree to disagree. Stevil - my position is pretty simple. Its the same as Ralph DeFronzo's which is that starting T2s on metformin is a waste of time. My position is also the same as Philip Home which is once you give the PWD all this crap in 5-15 years they will be on insulin anyway. diatribe.org/type-2-diabetes-start-early My position is also the same as what Al Mann said and why he invested $1B of his own money into afrezza's development which was put all the T2s on afrezza day 1. I wish someone can find the video of Al going at it with DeFronzo. Right now Mike has a study going on in India. It appears to be a redo of the Affinity2 trial. We already showed a superiority in Affinity2. My position is we need a head to head trial with Mounjaro for A1C and I don't give a crap about weight. I only care about A1C. My last position is we need to fix the ADA's SoC and if we can't just like Dave Kendall couldn't then Mike needs to work with another organization that is willing to do the right thing for T2s. |
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Post by prcgorman2 on Jun 9, 2022 7:22:27 GMT -5
Very interesting discussion. It would seem there is value in taking it to the next level. I don’t see that happening in the ADA Scientific Sessions. I do think taking the discussion to the next level could be done using conferences. Mike has claimed there are more than 3,000 prescribers of Afrezza. There are only about 5,000 endos in the US (and 225,000 PCPs) so it would be interesting to see what the ratio of endo to PCP in the prescribers would be, but I digress. Mannkind could host a User Group conference. Not the ASM, a User Group conference. Invite prescribers, users, VDEX, folks from Brazil, India, policy makers, INSURANCE PROVIDERS. It doesn’t have to be huge. A few hundred folks. Maybe double it up with annual sales training for the Mannkind reps. Talk about Technosphere. GLP-1s, breathing, BlueHale, maybe partner with UTHR and add a PAH/ILD segment. Do Birds of a Feather (BOF) sessions after cocktails and have open discussion on how to advance product and protocol development and treatment, and explore what people want to learn and know to help direct design, development, and execution of trials. We always talk about the PWDs as the customers, and they ultimately they are and it is their money that is getting spent (along with insurance providers). But the authorizers are the prescribers. It starts with them. What are THEIR needs? What do THEY want to know? The reps are hearing it, but is that good enough? Get Sam Finta and the guys who started their own user group in California (Sacramento) and underwrite their travel expenses. I guarantee the Mannkind management will learn a ton that will help them direct their efforts, and heck I suppose some of us investors might like to attend too. They should call the user group meeting the Mannkind Inspiration Conference (MIC). Get it? In physiology, inspiration is the process of inhaling. Come to think of it, there is an actual inhalable medication industry. It could become an industry conference which could help defray costs for venue and get more booths broader set of topics, et cetera. It could definitely be an additional positive catalyst.  |
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Post by agedhippie on Jun 9, 2022 12:06:32 GMT -5
... you say "I don’t know that Afrezza is weight neutral" afrezza is human insulin, nothing more. Its going to do what human insulin does. Insulin neither causes weight nor reduces weight. Caloric intake does that. However, the general belief is subq insulin cases weight gain which is not really the case. What happens is those taking subq insulin tend to snack more to balance their BG levels and with high BG the body is not converting the food you eat into energy. This lack of energy causes an increase in hunger so people eat more. This is wrong. You can see this is the recreational use of insulin amongst bodybuilders as a growth hormone. They use insulin as a means of increasing muscle bulk, but along with that bulk comes fat which needs to be burnt off. There is a whole sub-culture in body building around this (I used to get offers for my insulin at the gym which just felt weird!) This practice comfortably predates the arrival of RAA insulin. It has the benefit of not showing up on a drug test. The snacking more is somewhere between incorrect and mildly insulting. I do not eat more because I am using RAA - end of story.It would probably be better to move away from the idea that Mounjaro works by making people feel nauseated. This is a minor side effect and in most cases wears off as the person gets used to the drug not unlike the case of metformin (as well as a lot of other drugs). As with any drug some people don't adapt and they drop out. Mounjaro works on two fronts; it slows digestion which evens out the demand for insulin (the same way that the low carb high fat diet does although that uses fat to slow things), and by making insulin reclaim more effective so insulin circulates for longer and thus is more effective. ([Edit] Having read Ralph DeFronzo's paper now it appears to act on several other vectors as well) I do think Afrezza would be more effective (actually I think insulin in general would be more effective), but it comes with it's own baggage. Dosing is no longer once a week, but somewhere around 40 times a week for Afrezza and is time critical. This is going to be the obstacle to adoption vs. GLP-1, GIP-1, etc. in the general population. This then leads to the need to prove that the feature, fast insulin, translates into a quantifiable health benefit (my gut feeling is that it is, but I have not got the evidence to quantify it). If a risk is 1:1,000,000 then a 100% rise is a headline and 2:1,000,000, but it's still at a level where I don't care. |
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Post by agedhippie on Jun 9, 2022 12:26:43 GMT -5
I don't think we're getting anywhere as we're both seemingly firmly entrenched in our own sides. I think we may just have to agree to disagree. Stevil - my position is pretty simple. Its the same as Ralph DeFronzo's which is that starting T2s on metformin is a waste of time. ... Ralph DeFronzo's view is that they should all be on GLP-1 from day 1 since that addresses the broad range of the issues Type 2 causes leading to hyperglycemia. He would see Afrezza as deficient for first line use since it focuses on just the decreased beta cell efficiency and ignores the other issues. This is an interesting diagram from his paper ( diabetesjournals.org/care/article/40/8/1121/36799/Is-It-Time-to-Change-the-Type-2-Diabetes-Treatment). It also shows why he dislikes metformin - like insulin it only addresses one issue. In his view GLP-1 is far more effective which was the point Stevil was making.  |
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Post by sayhey24 on Jun 9, 2022 15:23:19 GMT -5
Aged - good comments. You are correct there is an entire sub-culture around using insulin with body builders and there is even the video with the guy using afrezza but insulin is what it is and its not IGF-I. These guys also lift a lot of weights and if they were not lifting the weights I bet the insulin would not be growing the muscle. The insulin helps as they get a boost in muscle protein synthesis and a decrease in muscle protein breakdown by grabbing all the glucose they can without passing out. They thing is they also combine it with anabolic androgenic steroids and that's what's building the mass. Thats your growth hormone.
The thing is too, the guy in the video basically says he has never seen an insulin like afrezza. It would be nice if we could get all T2 prescribing doctors to say the same.
We also have to give Ralph credit for being the father of metformin and pushing it through the FDA. We also need to give him credit for jumping on the GLP-1 bandwagon when that started paying the bills. How about we just do what the human body naturally does and not try to improve on nature and just give the body what it wants which is human insulin? I know there is not research funding in this for Ralph but I bet a lot of T2s would be better off with afrezza.
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Post by sayhey24 on Jun 9, 2022 15:49:27 GMT -5
Aged - you said "It would probably be better to move away from the idea that Mounjaro works by making people feel nauseated." To be honest I think the entire discussion on weight loss is a red herring in the A1C discussion but a good sales pitch from Lilly. If Mounjaro is that good at reducing weight after we dial in the afrezza dosing and get the PWD stable we can add the Mounjaro. However the tech diet companies are now starting to realize what we have been saying hear on proboards and that is the T2s are gaining the weight after they lose PPG control. Who knows maybe they will be the ones to start using afrezza before the GPs.
You said "Dosing is no longer once a week, but somewhere around 40 times a week for Afrezza" I really don't see that as an issue for at least 50% of the T2s. If they can pick up a fork to eat they can pick up a dreamboat. If afrezza got 50% of the T2 market it would be $10B+. Even at 10% of the market MNKD would be a $100 stock.
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Post by stevil on Jun 9, 2022 17:17:43 GMT -5
Stevil - my position is pretty simple. Its the same as Ralph DeFronzo's which is that starting T2s on metformin is a waste of time. My position is also the same as Philip Home which is once you give the PWD all this crap in 5-15 years they will be on insulin anyway. diatribe.org/type-2-diabetes-start-early My position is also the same as what Al Mann said and why he invested $1B of his own money into afrezza's development which was put all the T2s on afrezza day 1. I wish someone can find the video of Al going at it with DeFronzo. Right now Mike has a study going on in India. It appears to be a redo of the Affinity2 trial. We already showed a superiority in Affinity2. My position is we need a head to head trial with Mounjaro for A1C and I don't give a crap about weight. I only care about A1C. My last position is we need to fix the ADA's SoC and if we can't just like Dave Kendall couldn't then Mike needs to work with another organization that is willing to do the right thing for T2s. I don't like being a jerk, I just don't really have any interest in debating with you. It's nothing personal... I just don't agree with most of your scientific knowledge and find your arguments to be uncompelling. It would take a long time to read the information you've read and based off our cursory discussion of it, I'm not drawn to learn more about it. It is not consistent with my theoretical understanding of the disease at the molecular level nor does it align with what I see clinically. I won't go so far as to say that you're wrong because I don't possess the knowledge to do so. It has been a while since I dove head deep into the biophysical chemistry of metabolism, but from my undergraduate degree to medical school to now residency, the theory has been consistent. As has current research that our discussions have led me to use to refresh my memory. There's probably a great deal of information that I've learned in my education that will be proven incorrect in the future. I just don't think this topic is one of them... |
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Post by agedhippie on Jun 9, 2022 17:28:09 GMT -5
Aged - you said "It would probably be better to move away from the idea that Mounjaro works by making people feel nauseated." To be honest I think the entire discussion on weight loss is a red herring in the A1C discussion but a good sales pitch from Lilly. If Mounjaro is that good at reducing weight after we dial in the afrezza dosing and get the PWD stable we can add the Mounjaro. However the tech diet companies are now starting to realize what we have been saying hear on proboards and that is the T2s are gaining the weight after they lose PPG control. Who knows maybe they will be the ones to start using afrezza before the GPs. You said "Dosing is no longer once a week, but somewhere around 40 times a week for Afrezza" I really don't see that as an issue for at least 50% of the T2s. If they can pick up a fork to eat they can pick up a dreamboat. If afrezza got 50% of the T2 market it would be $10B+. Even at 10% of the market MNKD would be a $100 stock. TBH for me weight loss gets far to much attention and I am far more interested in how it impacts diabetes which gets buried by weight loss. My feeling is that Mounjaro is aiming to market itself as an all in one weight loss and diabetes treatment - one shot a week to lose weight AND treat your diabetes - total bargain... It makes me wonder how effective the diabetes side actually is. Trust me, there is a huge difference between picking up a fork and rooting through a bag to find the inhaler and some cartridges. Everyone is picking up a fork, only one person is burrowing in their bag  Dosing has to be somewhere between zero touch, and low friction. Any time you have to do something the option is there to skip it so the less interaction the better. People start out compliant and drift off as the doctors warnings wear off or there is no visible penalty or benefit. To be clear, it's not that I think Afrezza won't work for people with Type 2 (VDEX has proven it works well), it's that I expect like every other intensive therapy it will suffer horribly from compliance drop out in a less motivated population. |
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Post by sayhey24 on Jun 9, 2022 17:39:37 GMT -5
Stevil - if you don't want to debate, thats fine. Just don't respond. I am sorry what I am saying is completely uncompelling to you. I am just telling what DeFronzo said about metformin, what Holme said about in the end the T2 will be on insulin anyway and why Al Mann put $1B of his own money into afrezza.
I know this is not what you learned in school but its hard to argue with what we are now seeing with CGMs. I wish you the best of luck but when people are saying things which may not make sense listen. When I first met Al Mann he was saying all this stuff which made little sense to me either. One thing it did was challenge me to try and understand what he was saying and why. Maybe in the end Al was wrong. Maybe his understanding of diabetes was way off base. Maybe in the end Al's understanding was so screwed up he just wasted $1B.
One suggestion for you is to go back and read Al's old interviews and available interviews. Then ask yourself, why is he saying that.
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Post by sayhey24 on Jun 9, 2022 18:02:04 GMT -5
Aged - you said "It would probably be better to move away from the idea that Mounjaro works by making people feel nauseated." To be honest I think the entire discussion on weight loss is a red herring in the A1C discussion but a good sales pitch from Lilly. If Mounjaro is that good at reducing weight after we dial in the afrezza dosing and get the PWD stable we can add the Mounjaro. However the tech diet companies are now starting to realize what we have been saying hear on proboards and that is the T2s are gaining the weight after they lose PPG control. Who knows maybe they will be the ones to start using afrezza before the GPs. You said "Dosing is no longer once a week, but somewhere around 40 times a week for Afrezza" I really don't see that as an issue for at least 50% of the T2s. If they can pick up a fork to eat they can pick up a dreamboat. If afrezza got 50% of the T2 market it would be $10B+. Even at 10% of the market MNKD would be a $100 stock. TBH for me weight loss gets far to much attention and I am far more interested in how it impacts diabetes which gets buried by weight loss. My feeling is that Mounjaro is aiming to market itself as an all in one weight loss and diabetes treatment - one shot a week to lose weight AND treat your diabetes - total bargain... It makes me wonder how effective the diabetes side actually is. Trust me, there is a huge difference between picking up a fork and rooting through a bag to find the inhaler and some cartridges. Everyone is picking up a fork, only one person is burrowing in their bag  Dosing has to be somewhere between zero touch, and low friction. Any time you have to do something the option is there to skip it so the less interaction the better. People start out compliant and drift off as the doctors warnings wear off or there is no visible penalty or benefit. To be clear, it's not that I think Afrezza won't work for people with Type 2 (VDEX has proven it works well), it's that I expect like every other intensive therapy it will suffer horribly from compliance drop out in a less motivated population. I fully agree with you Lilly is positioning Mounjaro as the all in one treatment. I think its a brilliant marketing move and they will grab a big piece from Ozempic and the SGLT2s. The only thing that has a chance of impacting Mounjaro sales right now is afrezza but Mike needs to get aggressive and lets face it, its a hope and pray but Mike has the one tool which can impact it. I am not sure finding the inhaler in your pants pocket or on your kitchen counter is a big deal. After a few boxes you have more inhalers than you will even need. If taking a puff at meal time is afrezza's biggest issue then I hope that's a problem "Buzz" Harris can find a solution for. If thats our biggest issue I view that as a happiness problem. I know you want to downplay the fact that the Mounjaro participants were getting nauseated but they lost up to 8% because of this. Thats a big number. I think I would rather search through my pocket for the afrezza inhaler than lose my appetite because Mounjaro gave me a bellyache. BTW - I personally don't like shots nor sticking my finger for a meter test. If I could puff at each meal rather than taking the weekly shot I am taking the puff, but thats me. My dad could never give himself his own shots so maybe its a weird family thing. I also think if we can get the T2 early enough after 6 months many may no longer need afrezza at each meal. But, getting them all the CGM day 1 is key and if they are not taking the afrezza at meal time, you will see it and an automated email to their BF/coach will get them straighten out. |
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