Empagliflozin might be the best choice for the elderly, as it has significant benefits regarding CV disease.
From the paper: (Apologies if this has been posted before.)
“Empagliflozin should be considered in patients with type 2 diabetes mellitus and all forms of atherosclerotic CV disease to reduce CV mortality and hospitalization for heart failure.”
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Yes, Empagliflozin (Jardiance) is the best SGLT2I for the elderly and especially for diabetics who have had a heart attack. The biggest problem with it is the cost. My mother was prescribed it, but the monthly cost was outrageous in the USA (10X the cost of an Indian generic!). If it were not for my ordering her supply from India, she would have forgone using it. This highlights the deplorable state of American healthcare. Many drugs that are needed are suffering from price gouging for corporate profits. It’s beyond horrible.
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Indeed it is Chris. I’ve been ordering most of my medications from various other countries for 11 years. My physician is aware. I’m just a normal middle class American who worked in the medical field and on very few prescribed meds so my heart goes out to the untold number of people who don’t know this workaround.
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“paradox is that in T2DM, the glucose excretion threshold keeps going up as does glucose reabsorption”
Because T2DM is not lack of insulin but lack of insulin sensitivity, so the cells are actually hungry, the sufferers are always hungry despite having high blood glucose. Being hungry means…needing more sugar…
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Chinese paper.
Effect of dapagliflozin on metabolic dysfunction-associated steatohepatitis: multicentre, double blind, randomised, placebo controlled trial
“MASH improvement without worsening of fibrosis was reported in 53% (41/78) of participants in the dapagliflozin group and 30% (23/76) in the placebo group (risk ratio 1.73 (95% confidence interval (CI) 1.16 to 2.58); P=0.006). Mean difference of NAS was −1.39 (95% CI −1.99 to −0.79); P<0.001). MASH resolution without worsening of fibrosis occurred in 23% (18/78) of participants in the dapagliflozin group and 8% (6/76) in the placebo group (risk ratio 2.91 (95% CI 1.22 to 6.97); P=0.01). Fibrosis improvement without worsening of MASH was reported in 45% (35/78) of participants in the dapagliflozin group, as compared with 20% (15/76) in the placebo group (risk ratio 2.25 (95% CI 1.35 to 3.75); P=0.001). The percentage of individuals who discontinued treatment because of adverse events was 1% (1/78) in the dapagliflozin group and 3% (2/76) in the placebo group.“
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https://www.medscape.com/viewarticle/canagliflozin-cv-benefits-appear-be-dose-dependent-2025a1000fby
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Can someone who subscribes to the WSJ please post the full article:
https://www.wsj.com/health/wellness/diabetes-drugs-jardiance-anti-aging-6cc91047
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In mice: Empagliflozin Restores Cardiac Metabolism and Suppresses Immune Activation in Acute Myocardial Infarction 2025
EMPA restores cardiac energetics and attenuates the metabolic complications of AMI, independent of the presence of diabetes. These metabolic effects correlate with lower immune cell infiltration and cardiac necrosis, providing long-term benefits in AMI.
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“Is sotagliflozin a wonder drug?”
Also, does anyone know if it’s available from India?
Highlights.
Sodium-glucose co-transporter 2 (SGLT2) inhibitors reduce cardiovascular mortality and hospitalizations.
SGLT2 inhibitors reduce major adverse cardiovascular events.
Sotagliflozin improves glycemic control, reduces HbA1c, and offers weight reduction.
SGLT2 and dual sodium-glucose co-transporters 1/2 inhibitors show nephroprotective and neuroprotective effects.
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Well, I checked IndiaMart and couldn’t find it there. However, getting ahold of it in general seems tricky, insofar as it having been approved in Europe, but the company that developed it, requested it be not marketed in Europe anymore.
And I would not be looking forward to trying to get it prescribed in the US, and if successful, to then be subject to a grotesquely invasive walletctomy.
A pity, as it looks highly intriguing. In particular, the aspect of its primary distinguishing characteristic of substantial SGLT1i, along the axis of restricted uptake of glucose in the gut lining and slower rise in blood glucose. Very valuable in my view. And many other benefits. But no data/studies showing impact on neurological outcomes, and being relatively new, no long term data in general. If not for practical obstacles, I would strongly consider trying it and measuring the impact on my biomarkers.
However, it does seem to be the first representative of a true dual SGLT2/1i (much more so than canagliflozin). Hopefully, there will be others developed, but who knows. And maybe India will get around to making it - diabetes and CVD mortality and morbidity rates are rocketing over there and they need all the drugs they can get, maybe they’ll consider it to be a good candidate to have in the armamentarium.
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Once I’m interested in a drug, I do as much research on it as possble. Certainly sotagliflozin is an intriguing drug, due to its mode of action. Sometimes I post what I come across, if I think it might be of general interest.
Here’s an article that looks at the somewhat tortured and controversial process of FDA approval for this medication. The writeup here is not enthusiastic and rather skeptical. There’s a lot of emphasis on the paucity of outcome data, and some significant risks in certain patient populations. Of course this is just one particular take, and by no means dispositive, so I’m posting it in that spirit.
Heart Failure Drug Rejected, Rejected Again, Then Approved, What’s Up?
"It’s important to note that the clinical trials didn’t actually show that they’ll help you live longer.
“I want patients to be aware that the reason that we’re treating them with Inpefa is because the primary endpoint looked positive. The primary endpoint was supposed to be fewer deaths, but the new one, based on the shorter trial time was a sum of cardiovascular death, plus hospitalizations for heart failure, plus urgent visits per heart failure,” says Dhruva. He emphasizes that the trials did not demonstrate that people who took Inpefa were likely to live longer than those who did not.
“If I was counseling a patient, I would say there is uncertainty if this medication will help you to live longer. It’s possible, and I hope so…but I would like to see data before that claim is made.”"
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Preprint, in mice but NYU + Ann Arbor + UTHSCSA: Canagliflozin reprograms the aging hippocampus in genetically diverse UM-HET3 mice and attenuates Alzheimer’s-like pathology 2025
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Rich Miller is on that paper, so it’s from the same folks at the ITP. Highest quality stuff IMHO.
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I ordered some empagliflozin from India to experiment with as a geroprotective and for what it might do to maintain kidney function. My HbA1c has hovered at the borderline of pre-diabetic throughout my 70s. It has not progressed but it would be nice to see it drop a little as well.
I thought I would start with 5 mg/day and see how that goes. Does anyone who has experience with empagliflozin have suggestions about how much and when to take the drug and what side effects to be aware of?
I take 12.5 mg daily. Side effects are weight loss and extreme thirst for me. Pretty benign.
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I’ve been prediabetic for the past 10 years or so (A1c 5.7-5.9). I have never been overweight and my diet and exercise habits have always been very good. Male, 67 yo.
I started out with empagliflozin 12.5mg/day. Also from India, but original manufacturer, not generic. Initially, for several weeks, it seemed to bring my morning BG down to sub-100 mg/dL, into the 90’s and even occasional 80’s. Whereas ordinarily it was always in the 106-112 range in the morning (dawn effect). I used the same glucose monitor. However, after a few weeks, not changing anything else in meds, supps, diet or exercise, the BG drifted back to the original pre-empa readings. I was on this dose for 4 months. I tested myself at LabCorp, and the glucose readings were identical to pre-empa from 5 months ago: FBG of 108 mg/dL and A1c of 5.8%. Interestingly, the two tests were a before and after in the respect of in addition to empagliflozin, I changed from atorvastatin 10mg/day to pitavastatin 4mg/day and added rapamycin Eris/Biocon brand 6mg/1-week for 11 weeks. Yet zero changes in fasting glucose and A1c.
Kidney labs were essentially unchanged (for example serum albumin went from 4.8 to 4.7, creatinine 0.82 to 0.83 etc.). I didn’t do a urine test however. I did use a test strip at home to check that there was glucose in my urine with empa, and there was.
Subjectively I felt nothing different. No weight loss either (BMI of 21.4). No excess thirst.
It’s as if I took nothing.
I then upped the dose to 25mg/day. No change in supps, diet or exercise. However, I added bempedoic acid 180mg/day. And during this time I was coming off a rapamycin break (due to surgery), and then back on rapamycin for three weeks also 6mg/1-week, but Zydus brand. I was on the 25mg/day dose of empagliflozin for 39 days and tested again at LabCorp.
This time the glucose readings were dramatically different. FBG went from the previous 108 to 96, insulin from 14.2 uUI/mL to 8.6. I didn’t test A1c this time because it wasn’t 3 months yet between tests. However, a couple of things must be kept in mind. I was on the 25mg dose for only 39 days - and when I originally went on empa at the 12.5mg/day dose it also dropped my FBG in the first few weeks, but then drifted back up. It’s entirely possible that the same will happen in time with the 25mg dose. And while the kidney numbers were roughly the same, many other labs got substantially worse on bempedoic acid - however it’s likely a one off.
I continue on the 25mg/day dose and will test again early August with the only change being dropping bempedoic acid and going on ezetimibe 10mg/day for 50 days. I will also test A1c at that time.
As previously with the 12.5mg/day dose, I continue to not feel anything different subjectively, no weight change, no thirst etc.
If there is no change to my A1c of 5.8 or FBG above 100, and I continue to be prediabetic, I will add pioglitazone 7.5mg/day and possibly experiment with acarbose.
I take the empa dose first thing in the morning after I get up, hours before I eat, with water or tea.
Bottom line - in 7 months of empagliflozin on 12.5 and 25mg daily doses I have had zero subjective feelings of change, zero side affects, no weight changes, and no lab changes on 12.5mg, possible changes in labs on 25mg, but too early to tell, have to wait for a retest. That’s my n=1 report.
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I love it, thanks!
I’ve been on dapagliflozin at @2.5mg (cut the odd shaped pills) for less than one month and noticed pinker nail beds, less fluid retention if I eat a restaurant meal (from too much salt) and one unexpected thing for me is that it’s much harder to get into zone 2 or higher during exercise. I’m wondering if it has anything to do with the EPO boost I read about in this thread?
I’m not pre diabetic and haven’t done labs yet but I feel good on it.
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I take 10 mg empagliflozin every morning. No side effects that I have noticed.
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I have been exactly the same for the past 15 years. While a couple of doctors have described me as pre-diabetic, my fasting BG never goes above 115. For the last few years I have concluded pre-diabetes is a misnomer. There is nothing pathological going on. It could be due to physiological insulin resistance, where the body spares glucose for the brain and relies more on fat for energy in other tissues. In this case, fasting insulin and HOMA-IR can help determine if it’s pathological or adaptive in your case.I eat relatively low carb and my liver responds with gluconeogenisis. My insulin levels are excellent.
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