I think there is a place for SGLT2i in very specific patients, i.e. gout/hyperuricemia by lowering uric acid levels. Fasting, TRT, and sucrose/fructose (without acarbose) may increase uric acid. hyperuricemia levels are associated with diabetes, HTN, and CVD. High or low serum uric acid levels could be related to senescence and “inflamm-aging”
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I recommend you get a drugstore $25 blood glucose meter and measure it. It’s easy and useful for other purposes too. Heart racing and sweats at night could be a hypo or it could be a panic attack or something else.
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Thanks EnrQay, I do have a blood glucose meter and regularly measured my BG-levels. I ran out of strips, so I should just get some strips. You are definitely right I should measure my BG-levels when I experience a racing heart to be able to draw any conclusions.
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For me, the hallmark of hypoglycemia was a strange feeling from behind my sternum. Yes, my heart was racing as well and I had that sweaty feeling that you get when something is not right with your body. I am thinking of getting a CGM to measure this. It would help with my dosing of metformin/GLYNAC.
New Study:
Paper:
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I started to take Metformin after my fasting blood glucose has slowly been rising over the last 7 years from the 80’s to 115’s. While my FBG numbers really haven’t budged (still in the 110’s), but A1C has dropped from 5.3ish to 4.9 since starting Metformin. I have also wanted to take Met for anti-aging for years, so it was a good time to jump on. No doctor would prescribe it for me, so I went oversea’s route. Anyways, I take 1000 mg at night/dinner for about 9 months now (no side effects) and I have on hand Empagliflozin 25mg…have not started it yet. I got it for the same reasons of Metformin…anti-aging and the incredible protective benefits it has, but also for my blood sugar levels. Again, this is not prescribed. What/how would you dose this AND what are some protective measures to take for any possible, but rare, side effects?
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Another new paper - A review:
SGLT-2 inhibitors in patients with heart failure: a comprehensive meta-analysis of five randomised controlled trials
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)01429-5/fulltext
Good question. For healthy people, like most of us here, we don’t know for sure. There have not been any studies.
My approach is to try to use the lower dose, 10mg (but I also use the higher doses too, 25mg of empagliflozin). And I take regular breaks from the medication - I’ve used 5 days on, two days off as a starting point, but have no data to back up this dosing schedule.
Perhaps relevant to risk reduction strategies with sglt2 inhibitors:
Hmmm, the fact that I can check some boxes of the general risk factors and SGLT inhibitor-specific risk factors, does make me a little bit concerned. I do fall into the low BMI group and am a female, among others.
Have been taking Empagliflozin 10mg for a months now. Not sure if I should continue.
You may want to look at each risk factor specifically and see how relevant it is for you, and look at what can be done to minimize risk. And of course, discuss the risks with your doctor.
For example, people use d-mannose to reduce risk of UTIs:
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This was mentioned earlier by @rivasp12 , a paper out from the NIA ITP program:
Canagliflozin was found to diminish incidence or severity, in male mice only, of cardiomyopathy, glomerulonephropathy, arteriosclerosis, hepatic microvesicular cytoplasmic vacuolation (lipidosis), and adrenal cortical neoplasms. Protection against atrophy of the exocrine pancreas was seen in both males and females. Thus, the extension of lifespan in Cana-treated male mice, which is likely to reflect host- or tumor-mediated delay in lethal neoplasms, is accompanied by parallel retardation of lesions, in multiple tissues, that seldom if ever lead to death in these mice. Canagliflozin thus can be considered a drug that acts to slow the aging process and should be evaluated for potential protective effects against many other late-life conditions.
Full Open Access Research Paper here:
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Still seems so odd that it would have these wide-ranging effects in males only.
Here’s a good interview with ITP’s Richard Miller. I’m not sure preventing the glucose spikes is the whole answer with Acarbose and Cana. Why not work in females? Clearly they also have glucose spikes. That answer isn’t very satisfying. Is there some other pathway? Or maybe for some unknown reason males are more sensitive to glucose spikes and it does more harm. Totally unclear.
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As a female taking Empagliflozin, I’ve hoped for a while now that we would get some sort of answer to this question. Dr. Miller made some suggestions about this with regard to 17-alpha estradiol, but they still seem very much in the dark when it comes to Canagliflozin and Acarbose. Confusing to say the least.
I’m beginning to think that females are very responsive to rapamycin and the other drugs just can’t add much more to the benefits. With males there’s almost no limit to how much rapamycin and other drugs like acarbose will help them. They don’t max out with rapamycin like females.
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Acarbose and Canaglifozian have different mechanics of action, correct? Does anyone here combine these, or rotate them?
I rotate them. No need to double up with both of them, and risk of hypoglycemia if you do.
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Makes total sense. Have any particular rotation method?