Medtronic reps are salesman. Nothing works like they claim.
Congrats on getting such good results with the 670 system. Were your A1c’s leading up to starting the 670 much higher than your current numbers?
And some of them are sales ladies. SOME of what they say is true but can you imagine having to sell something that is so reviled by so many? They have GOT to learn the art of spin or they aren’t going to be successful salespeople. I feel sorry for them in a way.
Thanks Terry. I should have included that info. I hovered in the 6.8-7.0 range most of the time. Never better than 6.8.
I can certainly see why you like the 670!
… works for me it does.
For over 21 years MM/Medtronic has been telling me if I don’t buy their system I will die. Still pumping moved from H-tron to Animas, now on Tandem X2 and Dex G6 and Basal-IQ. Not doing bad for a 55 year T1.
Sorry to rain on the parade, but there is no foreseeable technology to replace insulin deficiency in the endocrine pancreas (i.e. diabetes of almost all forms). A pump, or injection, or inhalation, or anything known, is PERIPHERAL time-released insulin. It gradually drives the excess HGO (hepatic glucose output) supplied to the peripheral blood via the hepatic artery of the diabetic into insulin-sensitive tissues – especially muscle which can transform and store it as glycogen, and is large in mass.
In the islets, during the absorptive or prandial period, blood insulin and glucagon levels are up to 400 times those in peripheral blood. This is the location of the fundamental defect in diabetes, and where the portal nutrients are sensed by beta and alpha cells, and the only location in which an artificial closed-loop system could effectively replace or supplement the deficient insulin secretion of the diabetic, and prevent the excessive HGO that causes diabetic hyperglycemia (especially in its transient, acute or prandial form) due to prandial hyperglucagonemia, rather than simply compensating in the peripheral tissues by “clearing” excess peripheral blood glucose.
Any claim otherwise is BS, and anyone who does not understand the principles above is not qualified to talk about any existing or future diabetes technologies.
Meanwhile, CGMs are the next best thing. At least they alert the diabetic to the many events and conditions that can, and will, arise because of endogenous insulin deficiency and the lack of robust endocrinology of the non-diabetic.
Nothing wrong with one’s opinion but no need to bash on other posters with opinions which are not aligned with your own point of view.
Didn’t Medtronic’s “hockey puck” implantable pump inject insulin into the portal vein? I do not believe ANY of the pumps that currently purport to be ‘closed loop’ are being truthful. Sensors have a roughly 15 minute delay thanks to them measuring ISF. Insulin injected subQ is TOO SLOW to allow for fast enough of a response to be anything other than a STOPGAP feature until there is a pump that injects into the portal vein and a sensor that measures BLOOD, preferably arterial blood. I’ve had a lot of arguments with people over the many years that manufacturers have insisted on marketing their pumps as “closed loop”. IMO, the “loop” is not yet fully closed. It’s just a rough approximation, and a poor one at that. If it helps you sleep better to think that your pump is “automatic” and/or “closed-loop”, I say more power to you. We have not yet seen a truly closed loop pump and no one using their best argumentative powers will disabuse me of that opinion.
I wasn’t really responding to any other posters or commenters, but to the predominant misunderstanding of diabetic endocrinology in medicine generally. I would have hoped that that was clear by context.
Some people may be intrigued by a challenging statement, and investigate for themselves. There is an old saying about leading a horse to water vs. making him drink. So I intended to stimulate rather than offend.
Quit preaching as if to a child, why don’t you? As a T1DM parent, I suspect you yourself and your child could benefit hugely by understanding the endocrinology of the islet-liver axis. Do you? Do you want references from the research literature? I can provide them. You can start with the work of Roger Unger beginning in the late 1960s. Take a look at Alan Cherrington’s work too.
The health and longevity and quality of life of diabetics who adhere to standard medical guidelines will be unnecessarily degraded, I claim. Those who take the time to understand the well-measured/tested endocrinology will benefit immeasurably.
Insulin cannot predictably or reliably compensate for portal glucose (from dietary carbohydrate) in a diabetic – the negative/regulatory feedback of a non-diabetic is transformed into positive/unstable feedback in the diabetic, for GSIS (insulin) and hence for GSGS (glucagon).
Why don’t you challenge your own intellect and knowledge a bit more, rather than looking to pick fights, seemingly without any ammo? What I am writing has the potential to help a lot of diabetics – especially those willing to respond by investing some effort upon their own, and to learn. I can back up what I am writing, and invite concrete debate. I am too old, and life is too short, for me to respond to your opinion as to what I should and should not write in this forum.
It took me many years to self-diagnose my own diabetes and understand its behavior. During this time I came to recognize that almost all of the clinical research literature on diabetes is unhelpful (at best). I am trying to offer others a shortcut.
Again with the insults?
For what point?
If you’re saying that a pump, injection or inhaled insulin isn’t a good replacement for a fully functioning pancreas, I agree. I would take a good old pancreas any day over the current replacement options😀. But until then, I use the best tools available to treat.
I looked up the Medtronic device as follows:
This appears to deliver insulin via hepatic artery – not portally. It will not solve the problem of excess glucagon secretion by the alpha cells of the diabetic islets, and of the instability-inducing positive feedback of the diabetic’s endogenous glucagon response to portal glucose.
More fundamentally, it is only a pump. It is the islet endocrine response to portal nutrients that is unbalanced (for AAs) and deranged (for glucose) in the diabetic. In other words, any pump must be driven by a control signal. Both nutrient sensing and hormone delivery is in the portal vein endogenously. Both sensing and delivery would have to be portal for an effective medical device to fully correct or compensate for diabetes.
Even if the Medtronic pump were to deliver insulin portally it would not make a significant functional difference, and my original statement is valid.
In the lab canine models are most commonly used for portal access by researchers of islet endocrinology. That is because the anatomy of rodents is much too small, and hence unworkable. I don’t know more details of why, but I think location of anything (sensing or delivery) in the portal vein is a very difficult problem.
Even the so-called Biostator (artifical beta-cell machine), I think, is entirely periphery-based.
P.S. The phrase “closed-loop” refers to the combination of the nutrient-sensing and the hormone delivery, within a system. An open-loop pump, which I believe the Medtronic device is, would be programmed for a certain delivery rate independent of any nutrient sensing, and even independent of BG sensing.
Hence, even a closed-loop system based upon BG sensing is not even close to a functional replacement of the endogenous system of a non-diabetic, which responds to portal nutrients during the absorptive interval.
P.S. The fundamental defect, and compensating for it, has NOTHING to do with SPEED of administration or flux rate into peripheral blood. Nothing whatsoever!
Slowness, or speed, is a purely marketing-driven term but has no value in regulating blood sugar for the diabetic.
Dietary carb CANNOT be compensated for in any predictable or reliable way, due to the inversion of response (negative to positive feedback, or attenutation to amplification to use alternative terms) intrinsic to diabetes (excepting MODY-2, for which there is no secretory deficiency – it is a benign condition requiring no intervention). If you think a higher flux rate or lower lag time (from injection to initiation of flux) is a worthy goal, you don’t get it. That is, you do not understand the fundamentals of the endocrinology. Read the research out of Roger Unger’s and Alan Cherrington’s labs.
This is a good starting point:
One needs to understand the role of glucagon in diabetes, first and foremost.
Very interesting and thanks for the info!
It’s awesome. I’m a T1 adult. They didn’t have the screen sharing for the 670G at first, so the phone connection. But have come out with that feature so now you can.
I love the fact that it adjusts your rate intuitively and also that it kicks off the microbolus or basal rate if not in auto-mode) once you reach a low threshold. That’s such a safety. So if I happen to sleep through an alarm or lose consciousness, I’m not going to keep giving myself insulin if I am hypo. That’s just emergency care.
I like how much less hands on I need to be about corrections and constantly trying to calculate the right doses/corrections. It is able to predict if you are trending high or low and be proactive to keep you in range!