Has anyone else read this 4 year study?
In short two patients started taking insulin right away, vitamin D3 and sitagliptin.
Over 4 years they are off insulin and have improved c-peptide/GAD65 numbers.
I’m just curious what others think of this small example. This treatment is very similar to mine and so far working well.
Are you saying that you, too, are in remission by taking insulin, D3 and sitagliptin (Januvia)?
At a guess it seems like this treatment if started at diagnosis/during honeymoon may be de-stressing insulin producing cells enough to slow degradation. If I or my kid had just been dx’d I’d want my dr to know about it. Both patients in this study were over 18. Not sure if there are issues about giving kids sitagliptin (Januvia), which is usually prescribed for T2.
No definitely not saying I’m in remission. I’m just hopeful that small studies like these might be onto something. I am taking Tresiba 7U per-day, Fiasp 3U per-day, Januvia, Vitamin D3 and Jaridance. At diagnosis my A1C was 13%, 3 months later 5.7%.
Recently I’ve had to reduce my insulin a little because its been making me too low.
If you search for DPP 4 inhibitors and D3 you’ll find a few small studies that have had positive results in early treatment of type 1/LADA.
https://clinicaltrials.gov/ct2/show/NCT02407899
Sometimes I see these smaller trails show positive results and wonder why larger trials don’t take place to better prove/disprove their effectiveness. DPP 4/D3 is a pretty same combo for most people.
My doctor said they are only going to recheck my antibodies/c-peptide after a year so it will be a while before I have better evidence for how much this treatment is slowing my diabetes progression. All I can go by now is how much medication it takes to maintain a good A1C.
The little I can gather from lots of reading is early intervention with insulin and medications can slow data type 1 especially in adults who tend to develop more slowly.
It does seem like there’s more willingness to try “off-label” treatments designed for T2s on T1s. I’m T1 for 35 years, so not exactly a candidate for early-intervention treatment, but about a month ago my endo started me taking Jardiance @ 1/2 the smallest dose and it has had a big effect. It’s lowering my TDD by ~25%, helping to reduce my post-prandial spikes, and as a consequence making it easier to manage exercise without hypos. I also take Metformin, which I started back when I was on MDI to help control dawn phenom.
I’m a firm believer in the principle that the less insulin you have to take, the easier it is to manage. I hope you keep us posted on whether your treatment seems to be slowing the progression.
Hi Chris,
This might well be the case, and it is something I have discussed with my doctors (since I’m in the very-slow-developing T1 category). But, there is something to be aware of about LADA. The earliest clinical descriptions and studies of latent autoimmune diabetes in adults documented many cases where such diabetics had periods between six months and 15 years before they became insulin dependent.
The problem with small trials like those you link is that it is hard to get at mechanisms and causes and conditions. It’s possible that sampling error caught some LADA with very slow developing beta cell decline. I mean, if you were to look at my labs and clinical reports since 2015 you might conclude that the combination of Metformin, D3, and exercise has cured my diabetes, or put it in remission, or etc. My A1c dropped down to 4.8% within three months, and has since stayed firmly in the 4.6%-5.2% range.
However, that doesn’t mean much, really. My grandmother and brother presented almost identically to myself: very slow-onset, initially mis-diagnosed as Type 2, slowly but surely marching to insulin dependence, with antibodies showing up in testing later. My youngest brother just became fully insulin dependent (basal + bolus) fourteen years after being diagnosed at 22 years old. It looked for years like Metformin, D3, and Olympic Weightlifting was working for him too 
And then it wasn’t working anymore…
Anyhow, I’m not trying to discourage your bigger idea, just adding some info to the conversation. One of the nice things about science is that these small trials and experiments do get picked up and turned into larger trials eventually if they tend to show positive results. But, there is a reason for the delay in the way the process usually works:
Small trial/experiment/lab reports clinical improvement from off-label, combination therapy, or other “out of the box” treatment regimen;
Scientists equipped to do larger trials look at results and go “huh, interesting…let’s see what happens,” but don’t commit funds or retool labs without further corroboration;
Another report or small trial pops up, suggesting modest success with Amazing New Treatment X;
Big labs look at the methods, the results, the data, and conclude there is no known mechanism by which Treatment X could possibly be producing the results, and assume it’s statistical error until further evidence accumulates;
At this point in the process it tends to fork:
The fourteenth small trial held at SE Watushnuc State University and several long-term follow-up studies have very negative results–turns out the patients weren’t in remission or something else was responsible;
Big labs breathe a sigh of relief and assure their investors that they knew Treatment X wouldn’t work and were so smart they didn’t waste millions of dollars on large-scale studies;
People write off Treatment X as a footnote in clinical history.
Or
The fourteenth study is positive, and the four long-term remission cases are still in remission;
Big Pharma Lab #245,584 Senior Manager says “hey, let’s do a big follow up, and make sure Dr. Frank starts looking into previously unknown mechanisms for how Treatment X could possibly lead to remission…also, make sure you hire Dr. Barbara who did the first small study, we can always fire her if it doesn’t work out;”
…
Profit (it is Big Pharma, after all)
Even though I’m being hugely reductive, this really is pretty normal in science. If DPP4+D3+basal insulin turns out to have very positive effects in more small studies, one of the giants will absolutely fund both large trials and fundamental studies into the biochemical mechanisms. Ultimately, correlation without an understood mechanism can’t really be interpreted as causation.
Though sitagliptin comes with some risks, such as possible links to kidney failure, pancreatitis, pancreatic cancer, and severe joint pain, so using that for prolonging the honeymoon in suitable patients involves a risk/benefit calculation.
Also, those of us with established cases of diabetes can count on the chances of a cure going to zero once the disease can be prevented, since the public’s interest in addressing our plight would probably vanish if the disease were seen as preventable.
I do worry if they could prevent it there might be less investment in curing those already affected.
I suspect that the type 1 is caused by many factors and a cure isn’t going to be one thing but something specific to each patient.
Maybe there will end up being further sub-types of ‘type 1’ that have different treatments/cures
David49 Thank you for the reply. I think everything you said is reasonable and probably accurate. For my self I’d be pretty happy I could slow down by beta cell loss buying time. It seems like if there is a cure it will have two parts.
I’m thinking if you retain enough beta cells you might only need to stop the immune attack. Basically meaning you only need half of the cure instead of both parts.
I am aware of those side affects and don’t mean to down play them. I just think for type 1 the side affects of sitagliptin are very rare and worth some risk.
Let me know when there is a cure that allows me to drink a milkshake (roughly 80 carbs) without insulin. I’m always a bit bummed when I go somewhere for a burger and I don’t get fries or a shake.
@Dave44 I really miss having smoothies but now in hindsight I see they are ridiculous in carbs.
Just my opinion as a biologist: there already exists evidence that there are different “types” of Type 1. There are, last time I checked, seven distinct antibodies associated with Type 1 DM (although only 5 or 6 are used diagnostically), and at least one version of T1 that doesn’t have a discovered antibody associated with it (that would be T1b, or idiopathic T1). Since we know that T1 can develop while one or more auto-antibodies are produced, that it also can rarely develop in those without known antibodies being present, and we know there are a wide variety of presentations (acute onset in childhood, acute onset in adulthood, “typical” LADA, and very slowly developing LADA), it seems likely that there are similar but different mechanisms underlying autoimmune processes leading to beta cell decline.
There is also some interesting evidence from genetic studies that there are many different “types” or varieties of T2 DM, and some of those have hinted at links between inflammation, autoimmune attack, and T2 DM onset. Put all that together, and, well…it appears to me that diabetes is likely a constellation of related pancreas disorders which all lead to deranged glucose metabolism. I think you’re absolutely right that if cures for T1 (or T2 for that matter) are ever found, they will not turn out to be universally efficacious.
Now, all that being said, my actual area of biological expertise is plant-fungal interactions and immunity in plants. Which means you shouldn’t trust my word on any of this haha. I’m traveling for work or would otherwise link to some studies, but if you look through my post history you can find quite a few papers linked on autoimmunity and genetics in diabetes.
Man, is that ever true. Before learning to carb count and look into the differences between glucose, fructose, etc., it was really easy to accept at face value that “smoothies are good for you, they’re all natural!” Then start looking up nutritional info and doing the math… my wife was drinking an “all natural healthy fruit and veggie smoothie” the other day that somehow managed to have more than 100 grams of carbs ;/ And it looked really good.