If taking metformin be cautious that high fat can lead to g.i. distress. I eat a mod carb, 150 ,mod protein. I exercise everyday,pool or walking plus lot of yard work in the season,shoveling in winter. I have had Type2 for 25 years. I think a balance works best for me. Don’t panic early on, take a bit of time and figure out what works for you. Nancy50
Jean - here is what the doctors will be following come 2019 http://care.diabetesjournals.org/content/42/Supplement_1/S90
Look at figure 9.1 and print it out. Ask yourself does this make any sense? This is a “Treat to FAIL” approach. The last step when everything else fails, which it will in many cases if you live long enough is insulin. The #1 cause of death in the U.S. is heart disease and the #1 cause of heart disease is diabetes. Why? Elevated BG. Studies show as little as 2 hours over 140 causing issues. Non-diabetics rarely spike over 140. Why?- robust first phase post prandial insulin release from the pancreas.
If insulin is the fail safe why wait would seem to be the question? The answer is pharma sales of these other drugs along with the insulin stigma of needles and fear of dangerous hypos.
I have an interview with Ralph DeFronzo some where talking about how bad the amputation issue really is with the SGLT2s. If I have time I will look for it and post it. More important they do not address the issue which is loss of post prandial glucose release. At least the GLP1s will flatten out the curve like your high protein diet. The afrezza will stop the spike and if properly dosed will mimic a non-diabetic profile with no needles and no hypo fear.
I haven’t read this before. Would you mind posting the source? I currently use Afrezza, and I’ve been considering trying metformin for a few reasons. I believe metformin is supposed to help with this, but I was unaware that Afrezza could. That may influence my decision, so I’d like to read more about it.
Jean just a reminder there are many of us long time T2 on diet and exercise only avoiding the problems with meds. I do have to compromise on food choices, but worth it for me. 10 years and A1c of 5.7 no meds (dx at 12.0)
A possible option if interested.
I was diagnosed as T2 possibly LADA age at age 63 fasting 335.
I was given the option of going straight to insulin or do serious diet and exercise modifications. (Not obese or inactive). I decide to find out what my body would do with diet and exercise only. Surprise, it worked, I have been well controlled for 10 years. I am glad I took the option of finding out what I could do whith out medication.
Just remember all diabetics as individuals may vary. There is no such term as “all diabetics are or all need to do one thing”
In my case high protein is the same as high carb my body is great a changing protein into glucose. You need to eat very low carb, just the right amount of protein for body repair and very high fat. That would make a difference.
Katers - the source is the 118 study conducted my Al Mann at Mannkind. It is no longer available online but my understanding is the former Chief Medical Officer from the ADA Dr. Dave Kendall who is now with Mannkind is in the process of re-releasing it soon
In simple terms afrezza mimics the robust first phase insulin release which is lost by all diabetics. Its the first thing which goes for both T1s and T2s. That robust release blocks the alpha cells signaling the liver to shut off production. Since no other diabetics med including the RAAs like Fiasp can not do this, afrezza is unique. It mimics a healthy pancreas. Metformin in simple terms really screws up hepatic functioning between the liver and pancreas. I personally find 2 fingers of bourbon before bed provides better control than metformin for me but again thats me and not a recommendation for others to try.
A 200 patient clinical pilot was just concluded. While this is clearly not a scientific study, its easy reading and actually mimics the results Al Mann was seeing in his approved studies. Three interesting points in the paper was to properly restore hepatic function getting off meds like metformin was needed, they saw people with long term raised BG’s threshold for hypos rising to around 100+ being not unusual, they saw no progression in the PWDS over two years once target time in range was met. Hope this provides some info. I expect Dr. Kendall will be presenting the 118 study updates at ADA2019
I am not a big exercise person and I know it would help my diet work better. I have a Shake Table (google “exercise shake table” I have the little red one). I use it once or twice a day for 10 minuets. They say 10 minuets is as good as an hour of running. I will report back on how well it works.
Several years ago, TuD’s Emily Cole interviewed a principal of Diasome, a company developing a molecule that could be added to exogenous insulin to direct that insulin to seek out the liver. (That video interview link, unfortunately, has disappeared. @Mila) This is an attempt to mimic the effect native insulin has in a gluco-normal. In a non-diabetic, first-phase meal responsive insulin is released by the pancreas into the liver’s portal vein.
The liver senses this greatly increased insulin level and responds by replenishing the liver’s glucose stores and it also inhibits the liver’s release of additional glucose to the peripheral tissues. Only a portion of the original first phase insulin release moves on to perform its function in the peripheral vascular system.
Diasome’s product was something called hepatic directed vesicules or HDV. When I do a search on this company today, the last entry on their website is dated July 2017. I’m not sure what happened to this effort. It sounded promising at the time.
I use Afrezza, too. Mannkind has written about the positive effect that Afrezza has on the liver, mimicking a first-phase insulin release in a non-diabetic. It makes sense in theory but I’ve not read anything additional about this idea in years.
I’m afraid I may have hijacked the thread. Perhaps there’s a way to split this into a new one?
So alpha cells in the pancreas signal to the liver that glucose should be produced, and you’re (@George44) saying that Afrezza blocks this signal? Since I have T1, I probably don’t have any alpha cells left, but my liver is still dumping glucose all the time. I’m a little confused about how any of it works in that case.
Thanks for posting the paper, @George44. An interesting read!!
This is very interesting. Does this mean that potentially, your basal needs could be affected by Afrezza because your liver will eventually need to dump the extra stores it’s accumulated while Afrezza was in action?
I’m finding an increased insulin resistance in the evening that’s not really explainable. I’ve considered going on metformin recently for this problem, and I’m trying to understand how all the different players/medications would interact with each other.
Sorry I didn’t read the whole paper you posted @Terry4. It’s highly technical, so it will definitely take some time for me to decipher what it’s saying.
Here’s a much shorter version of the story, from a July 2017 Diasome press release.
Diasome Pharmaceuticals, Inc., a clinical stage pharmaceutical company, announced today that it has received an investment from the JDRF T1D Fund to further development of liver targeted insulin, a major step toward helping people with type 1 diabetes (T1D) better manage their blood sugar after meals.
In healthy individuals, the liver is where insulin is first used in an effective and rapid way. But in people with T1D who take insulin through injections and pumps, the liver’s key role in glucose control is compromised. An insulin targeted to the liver would more closely mimic the body’s own mechanisms to even out blood glucose fluctuations, potentially resulting in safer and more effective control of blood sugar.
Katers - your basal needs most definitely should be effected by afrezza use but not because of the liver is going to dump extra glucose. In fact it is the opposite.
The liver will only replenish what it needs. If it did not release glucose it doesn’t need to replenish it. However, shutting off glucose dumping when eating is key to control and time in range. You need to stop the post meal spike and get back to your baseline asap. In a non-diabetic this is usually within 2 hours.
However, if you look at the STAT study results and Affinity 1 analysis presented at ADA2018 by Dr. Kendall, afrezza provides you the ability to reduce your baseline without fear of additional hypos. This is done by increasing your basal levels. Here is the STAT https://clinicaltrials.gov/ct2/show/NCT03143816.
This is also what VDex found in their clinical pilot. How far they pushed this I do not know. You would have to contact them to find out. I also do not know how many T1s are in the 200 PWD population of their pilot.
What’s your AGP look like and how does that compare to the STAT and what VDex is showing would be my question? An additional issue and maybe the biggest issue with afrezza is it is typically under dosed so the huge benefits are not seen. The VDex team saw this last year and started increasing the dosing which is supported by STAT.
That was an intersting paper - thanks. It seems this has already been obsoleted with afrezza’s ability to mimic the robust first phase release.
What am I missing?
That could be true, but I think there’s likely more to the Diasome hepatic directed vesicule story.
My A1c and AGP are considered stellar by most doctors, but I’m struggling with highs during the night where I need to wake up and dose, and often the dose doesn’t work. It seems like my insulin sensitivity just magically starts working again around 3-4 am. I am not at all being conservative with Afrezza during this time frame. Below is a typical AGP report. My last A1c was 5.1%.
I know that to most people my AGP report probably looks great, but it looks great because I’m having to wake up during the night to correct.
Lows below 60 are generally a result of my long-acting insulin, not a result of Afrezza.
If you look at figure 4 of the Vdex, the pattern is actually remarkably similar to mine with a pronounced peak at nighttime. My chart is just a little lower overall.
Kater - These are amazing numbers! You are a walking advertisement for afrezza. Its a shame other PWDs are not yet taking advantage of it.
Maybe split dosing the basal is an option if you are not already. Another is a patch pump. As I mention above 2 fingers of bourbon before bed as an early T2 works for me but I am not promoting this for others.
I think the metformin will screw things up as it messes up the hepatic benefits you are seeing with afrezza.
LOL… alcohol inhibits the release of glucose from the liver.
While they say we have lost the first phase of insulin response with T2D, my fasting insulin levels were quite high. I suppose I have plenty but it’s not working very well and with T2D, there is the insulin resistance factor, which will deplete insulin over time.
Jean - until you have an AGP like the above its impossible to know how your body is reacting over time and to different foods.
You say your fasting insulin levels are quite high. If so I would expect to see a sharp spike after a high carb meal but then you getting back to baseline in 2-3 hours. A non-diabetic is about 85.
If you have this spike a low carb diet can help. Dr. Bernstein has had great success with his diet by removing the post meal spike. A low carb diet plus the afrezza may be a better option if money is not an issue. Actually afrezza by itself with carbs in moderation are not an issue.
Don’t get hung up on the insulin resistance factor, If Joslin’s current research is correct it is viral based and the best way to address in addition to exercise is getting a near non-diabetic time in range. You basically need to blunt the post meal glucose spike for best results in keeping TIR.
Here is some easy reading on my bourbon and why it works for me.
That is good you found something that works for you. I wish I could eat more carbs etc.
Well I still don’t think it is a good idea to have too much protein if it is meat, but if it works that is great. I am not able to be active enough to ever do that due to D and other things. I lost alot of muscle mass going into first dka and have not really got it back, replaced with fat now I think.