I’m a T1 of 30+ years and have always been on a pump. It’s been great.
However, my endo recommended that I try Ozempic to see if I could obtain better control and possibly lose some weight. Holy cow, this stuff is great. I’ve lost 20 pounds (10 weeks), had tighter glycemic control, and had massive appetite reduction. I also feel great weighing less, and will enjoy the health benefits of weighing less.
I wonder out loud, if a lot of T2 medications (even as simple and common as metformin) would help me who was originally diagnosed as “Juvenile Diabetes” half a century ago, but i am way way past AARP eligible now :-).
Ozempic and Trulicity are higher tech but maybe even more applicable. Great to hear your success story! I will specifically be asking my endo tomorrow if any of these T2 medications might help me lose weight.
I haven’t tried Ozempic, but I’ve been doing the Trulicity thing. Same GLP-1 agonist class of medicine as Ozempic. About to start my final/highest dosage this week. (You start small and titrate up to minimize the GI side-effects.) I’m likewise loving it!
I’ve lost just over 10lbs in 3 months. It doesn’t sound like a lot, but it’s the most significant weight loss I’ve ever seen in my adult life. I only started at around 130lbs, but it’s more than I liked on my 5 foot petite frame. I’m steadily getting back to my happy place!
I’ve seen a significant reduction in my total daily dose of insulin and I’ve definitely noticed that it slows my carb absorption from meals. The post-prandial spikes are easily tamed. My appetite has been reduced, too. I’m very easily sated and never seem to have junk food cravings anymore.
I like that it’s a once weekly dose, but I hate the auto-injector syringe. I always feel like my skin is exploding at the injection site.
Wish I could control the rate of delivery myself. I’ve learned it’s least painful given in some belly fat, rather than my thighs.
It was the doctors over at TCOYD that first got me interested in trying out the Type 2 meds, despite being Type 1. I’ve since tried a few, and didn’t find any of them nearly as favorable as the Trulicity. Metformin didn’t do anything, other than upset my stomach. I tried an SGLT2 (the ones that make you pee out excess sugar), and wound up being allergic to it. Jardiance, I think it was. Still have the scars from the rashes. I took it for several weeks before I figured out I was covered in hives, not mosquito bites. (It was the hot, wet, and buggy session ) I didn’t find it very useful. I think it lowered the spill threshold to 160ish for me, and I just don’t spend enough time above that to be useful. I would have had to sacrifice control to reduce my insulin intake with it.
I’ve actually been completely off the Trulicity for a week, inadvertently. Too many timing mishaps, pressing projects, and procrastination this week to get to the pharmacy. I’m surprised at how much I miss it! I didn’t fully notice how much it was doing until I’ve been without it. Hopefully we’ll be able to pick it up this afternoon.
It’s my opinion that some type 1 DMs actually have the genetic profile that cause insulin resistance. I’ve heard this called “double diabetes.”
While type 2 DM like I have can never turn into type 1, it seems to me that just having beta cells destroyed by the immune system doesn’t mean the person can also have the same problem as most diabetics.
This would explain those T1DMs who have to use large amounts of insulin and have problems with weight gain. None of my T1DM friends are in this cohort, as they tend to be thin, but I know there are some, as @Jaybear, who is benefiting from a type 2 medication, even though he is a type 1.
@Luis3, I also find it very misleading that both T1 and T2 are called diabetes suggesting to many that T1 is just a more severe variant of T2. I think of insulin as the fat hormone. Insulin tells the body to put on some weight. I see it in myself. If I want to lose weight, I need to cut my insulin.
Insulin does a whole lot more than cause fat accumulation. Without insulin glucose cannot enter into cells to provide energy. Excess glucose gets stored in the liver as glycogen, but the amount the liver can hold is finite. Excess after that is stored in fat cells.
The key if one is using insulin therapy is to reduce dietary carbohydrates which should allow the reduction of insulin. However in people with insulin resistance it takes a lot of insulin to bring blood glucose levels to normal.
The following snip is all I get without registering with Medscape:
Insulin is an anabolic hormone that promotes glucose uptake, glycogenesis, lipogenesis, and protein synthesis of skeletal muscle and fat tissue through the tyrosine kinase receptor pathway. In addition, insulin is the most important factor in the regulation of plasma glucose homeostasis, as it counteracts glucagon and other catabolic hormones—epinephrine, glucocorticoid, and growth hormone. What is the function of insulin?
this is really interesting! I’ve been researching these meds and would love to lose a few pounds. My insulin use is quite low and TIR great, but curious to see how things would be different with this! or Trulicity as @Robyn_H mentions. Curious if either of you have had side effects or know of any risks for these meds? thanks!!
This is a video from the TCOYD team. They summarize the pros/cons way better than I could. The video talks about more than just the GLP-1 receptor agonists @Jaybear, @Gezunt, and I (among many others not commenting here) are using. It’s interesting and worth the full watch, though.
If you follow TCOYD, they seem to favor the SGLT2 inhibitors (Jardiance, Invokana, etc…). There’s even new clinical research on them that @Sally7 has shared her experience with. From what I’ve seen on this forum, though, they’re not nearly as well-received by us Type 1 guinea pigs as the GLP-1 agonists. As men who are much less prone to them, I think they undervalue the horror of yeast infections.
Robyn: Thanks so much for posting this video! This is information that every Type 1 should have. I’m lucky that my Endo is progressive about my treatment and willing to prescribe traditional Type 2 drugs because of their benefits to us Type 1s. THANK YOU!
I’m also a long-time T1 doing well on Ozempic, and I’m excited to see there’s a growing number of us!
I tried metformin first, and it cut my post-meal spikes by 50% and made my DP way more manageable, but it eventually (after 6 months or so) started giving me such gnarly heartburn I couldn’t even tie my shoes anymore (among so many other challenges), so that ended that. I think I lost a few lbs with it, but nothing notable.
After a year or two of just insulin again, I got to try Victoza and I feel in love with it almost instantly. My BG was mellower- highs were lower and lows were less frequent because i wasn’t chasing so many highs, no obvious side effects, and I just felt like my entire body- every organ, every cell from my hair to my toes- was working more smoothly on it.
Eventually my insurance decided Victoza was outdated and forced me to Ozempic. I certainly like it enough to keep taking it, and its got all the same bloodsugar effects that Victoza did, with the added perk of being 10lbs down even, but I feel like Victoza and I were a perfect-made-in-drug-heaven-match and Ozempic is merely “really useful”.
(I tried explaining my love affair with Victoza and how good it makes me feel to a friend in med school hoping she could help give me better vocabulary to explain it, and she thought I had mostly grown a second and third head by the time I was done raving about how everything is better with Victoza’s wonder juice formulation coursing through my veins.) I’ve got no idea what might actually be happening in a physiological way when I take it, or why my response to it seems to be so much more whole-body-and-mind than just better BG control, but if I win the lottery, Im switching my Ozempic back to Victoza just as soon as I can! Still grateful to have access to Ozempic since its totally working for my BG needs, though!
It’s actually the exact opposite, to my knowledge. Both the GLP-1 RAs and SGLT2 inhibitors are presumed to have the same cardiovascular benefits in Type 1s as they have in Type 2s. Though I know of no study specifically stating this, as it’s hard to obtain long-term data en mass for the limited Type 1 population, compared to the Type 2 population. It’s only theoretical based on the mechanism of action. I’d certainly like to see any such study if you can find it, though! I wasn’t able to find any such study myself with creative Googling.
The SGLT2s are approved for Type 1s in many countries outside the US, but not in the US. There is no “prohibition”, though, they’re just not indicated for Type 1s. Meaning drug manufacturers can’t market to Type 1s, but doctors are free to prescribe drugs “off label” at their own will.
When I mentioned that I feel like the TCOYD doctors favor the SGLT2 inhibitors, it’s because I’ve heard them say many times over that it just wasn’t the right time to present the SGLT2s for use with Type 1s to the FDA, and they except there will quickly be clearance for them. Basically at the time, improved TIR wasn’t considered a credible finding as A1c was still the only benchmark of value, and even the slight risk of DKA was too much to justify marginal A1c improvements. They’ve even done a video wholly devoted to them.
If you’re interested in Type 1 specific studies, this is a great publication summarizing the limited work done:
You can can scroll down to section 4 to read about the risk of DKA, and section 5 is all about the perceived cardiovascular benefits and why they should apply to Type 1s also.
But yes, it boils down to Type 1s needing to use them responsibly, and the prescribing doctor is the only one who can judge whether or not a particular patient is able to do so. And unfortunately, those who would benefit the most from them (people who spend a lot of time over 160 mg/dl) are the most prone to suffer DKA. The risk of DKA lies in not knowing you lack basal insulin. As in, not recognizing a pump failure because your sugars never got crazy. Or not noticing you forgot your long-acting insulin dose because again, your sugars not got crazy. I basically had to promise to pee on a stick anytime I got queasy, but aside from that, it was easy to convince my doctor to write the script because she trusts me to self-manage. I’m just not a fan of the one I tried. It’s another “too little, too late” scenario, with heavy emphasis on the “too late”, in my opinion. The GLP-1 RAs seem like a better proactive tool, whereas the SGLT2s do most of their work on the backend, after your BG is already elevated.
The study was one I signed up to participate in about six years ago in the UK. We were awaiting the go ahead after all the prelims had been completed when it was announced by the pharmaceutical company, I think it was Boehringer, that they were discontinuing the study as earlier participants had had too many unfortunate side effects to continue. I know it was in the news but that’s all I remember,ber.