The State of T1D Outcomes published


Type 1 diabetes is a complex sinister disease. Every person diagnosed is very individual and the disease generally affects every single internal organ and hormonal system in the body. Even with CGM technology, pump technology, newer insulins, and far fewer finger sticks, managing Type 1 diabetes is a major pain in the behind. I have to count carbs or carb equivalents for everything I stick in my mouth.
Lack of money, lack of time, lack of T1 education, the obnoxious duty of managing refills, avoiding lows at work and during exercise, avoiding DKA when sick, checking your feet every single day, makes T1 a full time job that no one ever wanted. I’m actually surprised the 2016 to 2018 looks as good as it does, which in reality doesn’t look good in the least.
I’m doing much better than average and was one of my previous endo’s favorite T1 patients. Yeah for me! But for the rest of the T1 population, it’s a long, tedious road.


I agree. The medical communities ignorance is what is preventing those using the new available technologies from getting better results. They are happy if your HbA1C 7.6. They are concerned if it’s below 7.And I believe it’s helpful to adjust your diet to reflect how insulin works as well to prevent some of the complications of overeating.


@Mary67 - Unfortunately the majority of doctors fear lawsuits if their diabetic patients fall victim to extreme hypos based on their advice to run blood sugars in the 4.5-5.0 (80-90 mg/dl) range.

My doctors (both GP and Endo) strongly oppose the idea of my A1C being in the 4.6-5.0 range, but I no longer pay attention to them as their advice is based on patients using non-analog insulin, administered via MDI with no CGM’s. That and I don’t consume carbs so blood glucose peaks and troughs longer occur.

As @Terry4 would say, my 55 years of living every day with T1D (480,000+ hours) far exceeds all the schooling and time they’ve accumulated dealing with the ups and downs of daily life as a diabetic.


For anyone with diabetes who has paid attention to their glucose metabolism, the chasm between your experience and the doctor’s is huge. The notion of a doctor or endocrinologist as a “high priest of diabetes” took a long time for me to displace in my mind. Our deep experience gives us a platform that most people with diabetes and certainly the credentialed medical professionals do not appropriately value.


I think it’s worth reiterating, because after years—some of us decades—using insulin we tend to forget how unusual this situation is. I can’t think of any other disease where the patient has to dose herself with a dangerous, potentially deadly prescription medication multiple times a day for years on end, without direct medical oversight. It’s easy to forget how this looks from their p.o.v. They have to let us do this; there’s no other practical way to manage it. But it goes profoundly against the grain of their training, all the way back to “Do no harm.” And whereas in a self-selected group like this we may feel justified in resenting being nannied about this stuff, a lot of people probably shouldn’t have drivers licenses much being left to their own guesswork in injecting substances as unpredictable and powerful as insulin into themselves not just once, but thousands and thousands of times over the course of their post-dx lives.

ETA: Of course I’m mainly speaking of those of us who have the disease, versus parents, especially of little kids with T1. I think they generally have a much keener awareness of what a crazy-scary thing it is!


This is a good observation. For those who wear a continuous glucose monitor, I recommend a simple rule fo thumb to reveal appropriate glucose targets.

Glucose variability is the key to safely lowering a glucose average. If your glucose variability as measured by standard deviation (SD) is say, 50 mg/dL (2.8), and you consider 70 mg/dL (3.9) as your hypo threshold, then your blood glucose target should be no lower than 120 mg/dL (70 + 50) or 6.7 mmol/L (3.9 + 2.8).

If you can consistently reduce SD to 30 mg/dL (1.7), then it is reasonable that you can set 100 mg/dL (70 + 30) as a good glucose target or 5.6 mmol/L (3.9 + 1.7).


I’ve been puzzled for years wondering how he thought he could advise me on changes I should make by a one minute look at sugar averages over three months. Anyway CGM has got me closer to where I’d like to be. And tweaking diet to eliminate most grain carbs helps with the highs


Wish I could find an endo with type one. Maybe that would be helpful.


@Terry4 @ChrisP - I completely concur with Terry regarding glucose variability (aka Standard Deviation). It’s not rocket science. Std Dev simply measures how little or much your blood sugar varies from your daily average.

In the mg/dl world, this means your Std Dev should be less than 1/3 your average. If Avg = 120 mg/dl, Std Dev should be < 40.

I’m in Canada, so my measurements are all in mmol/L (multiply by 18 to convert to mg/dl). My target blood sugar is 4.6 (83 mg/dl), and my target Std Dev is now below 1.0 (18 mg/dl)


Two years ago I would never have dreamed of running sugars at this level (back then my A1C’s were high 5’s or mid-6’s). No one ever told me about ultra-low carbs, which led me to Keto. The only time I’ll ever spike (higher than 7.8 (140 mg/dl) is when my infusion site goes bad.

I miss all sorts of carbs - breads and pasta especially. But I’ve found keto alternatives, and I love the fact I’m no longer on any BP meds :+1:t3:


Nice illustration of using BG variability as indicated by standard deviation as a way to determine safe BG targets.

I’m going to edit my earlier comment to add the mmol/L context. A < 1.0 mmol/L (18 mg/dL) standard deviation is awesome. Keep up the great work.

I eventually lost my fond feelings for some of my historic high carb comfort foods. I value good glucose numbers and the way they make me feel so much more than historical habit.

When I quit smoking, instead of thinking longingly about how good a cigarette tastes, I forced myself to think about how really disgusting it is. I imagined myself licking an ashtray and that helped with my motivation.


Over the past 16 years much new technology has been applied to treating T1D. New insulins, CGM, better pumps, cloud reporting of data, online forums. If all spending for T1D therapy were to have grown 4.4% per year over that time period, it would be twice as high today – a not unreasonable guesstimate. And yet, HbA1c control is no better today, and is actually worse in some groups. How can that be!!!

There is one possibility: perhaps our understanding of glucose metabolism and T1D pathophysiology is incomplete. Perhaps we’ve pushed the insulincentric model as far as it can go. Perhaps we’re missing something…


I think the unfortunate fact is that controlling Type 1 diabetes is just very, very hard. Those of us on this site are highly motivated to maintain tight control, and even we struggle quite a bit. There are some that are unable to hit A1c levels that others have been able to maintain for years, and not for lack of effort.

I think the automated systems that are coming in the near future will have a major impact on these types of statistics, allowing people to achieve tighter control with less effort and fewer lows.


Perhaps you have answered the question.


The worsening A1c looks to me to be primarily driven by young adults rather than children (at first glance at charts, without diving into the actual numbers). I’d be willing to bet that the incredible increase in costs associated with rising insulin prices, expensive CGM and pump DME and supplies, etc. are partly to blame for this.

I suspect that for many, many young adults and teenagers, treating their diabetes effectively is just becoming too expensive compared to even a decade ago. In the U.S., poverty rates are directly related to age (children and young adults are much poorer than middle-aged and older Americans), and as the rest of the report shows, socioeconomic status is directly related to outcomes.

Anyhow, I suppose this is all obvious, but didn’t see any cogitating regarding the reason their has been an increase in average A1c in those age groups. My guess is costs associated with modern insulins and DME.


Only clinical research can definitively answer the question. However, it seems to me an hypothesis starts with considering the fundamental cause of T1D: destruction of pancreatic beta-cells. So, the basic concept of treating T1D is to restore (substitute for) the metabolic function of these cells. Are we actually doing that? Are we missing something?


Perhaps there might be hope on the horizon?

Dr. Paul Laikind is the President and CEO of ViaCyte, (, a company that aims to develop “a product that can free patients with type 1 and type 2 diabetes from long-term insulin dependence.”


Viacyte is working on a truly Big Idea, and Paul is the guy who can make it work, if anybody can. Meanwhile, it would be nice to have additional eggs in the T1D basket, since all clinical research is highly risky.

To consider an alternative, let’s focus on the main physiological barrier to effective insulin therapy: hypoglycemia. If T1D patients had normal responses to falling blood glucose, severe hypoglycemia could never occur. If hypoglycemia were never a risk, insulin therapy aimed at bringing HbA1c into the normal range would be simple.

The cells which respond to hypoglycemia are the alpha-cells, and except for the lack of a proper glucose counterregulatory response, alpha-cells in T1D appear to be relatively normal. Some researchers have even proposed that glucagon is more important than insulin in the pathophysiology of T1D.

So, why do alpha-cells stop secreting appropriate amounts of glucagon in response to hypoglycemia?..


That is their main function, but they don’t perform it.

It’s like saying - other than my car not working, it works great.


@Ted_Greene @Eddie

Alpha cells don’t lose their ability to produce glucagon, rather the synaptic feedback loop stimulating its production is altered or blocked. Some believe it’s blocked glutamate receptors, which are thought to be part of the glucagon feedback loop.

"The molecular mechanisms regulating glucagon secretion are still poorly understood."


I think you’re headed in the right direction, Jim, but I’m not sure I understand what you mean by “synaptic feedback loop.” Do you mean on a paracrine level within the islets? Between beta- and alpha-cells?

If so, I’m skeptical about that theory, which has been proposed by Cryer et al. They believe there is a “switch off” signal that triggers the glucagon response to hypoglycemia, and that the switch off mechanism is a sharp drop in insulin secretion by the beta-cells. This is plausible, because the beta-cells are absent in T1D, which would cripple that paracrine counterregulatory feedback. Their theory critically depends on demonstrating a direct insulin-suppressing effect on alpha-cells, and the data in this regard are confusing.

I think there is a more plausible explanation, which is based upon studies which indicate that the alpha-cell response to hypoglycemia is triggered via the autonomic nervous system. This strikes me as an attractive candidate, since brain tissue is the most sensitive to hypoglycemia. Without sufficient glucose, the brain shuts down, which is a serious, life threatening problem.

So, how does the glucose --> brain --> alpha-cell signalling work? And, why would destruction of the beta-cells interfere with that critical control loop?