I took 10mg Jardiance for 6 months which lowered uric acid from 4.5 to 3.3 and lost 6 pounds. No impact on FBS and A1c. I stopped because I am already thin and don’t want to lose the weight. May reconsider in future.
I’ve been using 10mg Empagliflozin for four years. No side effects besides a slightly increased hematocrit/hemoglboin which is only relevant since I’m on TRT.
I would imagine many healthy people here take a SGLT2 and you could make a case that they are #1 for longevity ahead of everything else in humans. Why not reduce your risk of all cause mortality if you’re not getting any side effects?
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You may want to consider pitavastatin. It doesn’t cause blood sugar issues. The equivalent dose of pitavastatin to atorvastatin 20mg would be 4mg. Easily available from Indian pharmacies. Regardless, I would not trade lower A1c for lipid disregulation. Lipid control should take priority. Fortunately, that is not necessary. There are of course also LLTs not involving statins as you well know.
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For what it’s worth I’ve been taking 10 mg / day of Dapa for a couple of months with zero issues. I’m not that muscled and I had an HA1C of 5.0 to begin with. AND it’s layered on top of 2.5 mg tirzapetide, recently switched to 2 mg of Reta. No symptoms whatsoever. ChatGPT told me that dapa is gentler than empa hence my choice.
Just to throw in my 2 cents, I am in my 50s and train very hard and compete athletically in an amateur capacity. I have had to try different protocols but basically settled with this: Jardiance 5mg (split pill) on AM non-exercise days, though walking a lot (even up to 10 miles or more, but not if doing zone 2) is fine on these days. Since the half life is ~13 hours I won’t take berberine or anything sugar lowering the day of jardiance and the next day (assuming will work out), but would 2 days after. I find that the washout is good enough for an afternoon or evening workout the next day, but if had to workout or race that morning instead would need to skip the Jardiance the day before. I can tolerate 10mg on a non-workout day, but the issue is the half-life / washout of which 10mg would not washout on time if exercising the next day. If I know I will be taking more than 1 day off in a row (usually don’t know, have to play it by ear), I can take 10mg on the first of the successive days off.
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We’ve had a number of threads on this topic… right now I’m less concerned about it because most of use here only have lower uric acid levels due to our SGLT2 inhibitor use…
A dose-response relationship was found for uric acid; individuals within the lowest quintile had almost twice the chance of reaching age 100 compared to those in the highest quintile.
Low uric acid due to SGLT2 inhibitors is generally beneficial or neutral . It reduces gout risk and may support metabolic and cardiovascular health. However, extremely low levels or symptoms like kidney pain or frequent stones might warrant further evaluation.
from: Is lowering uric acid useful for longevity? - #41 by RapAdmin
Other past threads here:
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This was about one year ago. My 62 score was normal… but not by much… my physician used this score to put me on Jardiance, covered by insurance. Will have an updated test in July 2026.
Creatinine is high because I take Creatine every morning and a second dose every other day before gym.
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No issue with 25 mg Jardiance 8 months.
Feel fantastic. I am shredded very little adipose tissue… 14% fat. BMI
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I’ve been taking Jardiance 25mg since January 1. Zero side effects. I drink a lot of water, infrared sauna 35 minutes daily, cardio and weight train. My bloodwork last week showed glucose 80, A1C 5.5. I also do intermittent fasting and take Metformin, usually when a day after a high carb meal. I take Lipitor twice a week and Ezetimbe daily. Lipitor has a three day half-life and my results are the same whether I take it five days a week or seven days a week or two days a week and tried them all. I’m 73 y.o.
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Deborah_Hall,
In answer to your question about SGLT-2s and bone remodeling I asked ChatGPT. Keep in mind that you can not have complete trust in this particular AI program which regularly gives me wacky answers. Here is my question, followed by ChatGPT’s answer:
SGLT-2 drugs can cause problems with bone remodeling: Search for evidence of this for each type of SGLT-2 drug. Note whether evidence indicates an increase or a decrease in bone density for each SGLT-2 type. Note whether there could be an increase or decrease in fracture risk due to bone remodeling for each SGLT-2 type. Put data in a table and use the minimum number of words to clearly answer each point.
Evidence is strongest for canagliflozin; for the other SGLT-2 inhibitors, bone effects are generally neutral or uncertain. Class-level meta-analyses show no significant reduction in BMD and no significant increase in fracture risk overall.
| SGLT-2 drug | Bone remodeling / BMD evidence | BMD direction | Fracture risk from bone effects |
|---|---|---|---|
| Canagliflozin | Most evidence for altered mineral metabolism; some long-term studies reported modest hip BMD loss. CANVAS fracture signal observed. | ↓ slight (hip; not consistently all sites) | Possible ↑; evidence mixed, not confirmed in later meta-analyses. |
| Dapagliflozin | Studies generally found no effect on bone turnover markers or BMD. | ↔ no meaningful change | ↔ no clear increase; isolated renal-impairment trial reported more fractures. |
| Empagliflozin | Clinical trials and pooled analyses found no meaningful BMD or fracture signal. | ↔ no meaningful change | ↔ no increase detected. |
| Ertugliflozin | Limited data; cardiovascular outcomes trial found no significant fracture increase. | ↔/unknown | ↔ no increase detected. |
| Sotagliflozin | Very limited direct bone-remodeling data. | Unknown | Unknown; no established signal. |
| Drug | Bottom-line assessment |
|---|---|
| Canagliflozin | Weak evidence for ↓ BMD and possible ↑ fracture risk; strongest concern in class. |
| Dapagliflozin | Neutral BMD; fracture risk generally neutral. |
| Empagliflozin | Neutral BMD; fracture risk neutral. |
| Ertugliflozin | Neutral/insufficient BMD data; fracture risk neutral. |
| Sotagliflozin | Insufficient evidence. |
Overall class conclusion: SGLT-2 inhibitors do not appear to decrease BMD or increase fracture risk as a class; concern is mainly limited to canagliflozin, and even that signal remains debated.
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I started Jardiance 12.5 mg with breakfast about 9 months ago. It consistently lowers my post meal glucose spikes and it brought my HbA1C down from 5.7 to 5.4. I notice no side effects except possibly a slight decrease in energy level, but I don’t want to take the time to test that theory.
Yes, glucose in the urine is a very slim potential problem, but highly unlikely for anyone maintaining regular hygiene. Having said that I suggest you look up SGLT-2 inhibitors and Fournier’s gangrene (necrotizing fasciitis of the perineum), a rare but potentially life-threatening infection.
Jay, thank you so much for the information. Looks like empagliflozin might still be something to consider.
Empagliflozin actually raised my glucose levels, slightly. I’m 46, relatively lean (14-15% body fat), and already have pretty low fasting glucose. My fasting glucose taken from blood panels has ranged from 67 to 83 mg/dL since 2023, my A1c has ranged from 5.4 to 5.1 during this time as well. My A1c goes up or down primarily depending on how much I eat and how many carbs I eat; same for my fasting insulin levels, which go low the less carbs I eat. So, I decided to experiment taking 10mg of empagliflozin daily, typically at night for about 90 days. During the last two weeks I put on a Stelo CGM and recorded my glucose values, then stopped taking it, and put on another CGM. I suspected that the empagliflozin was raising my glucose levels already, because when I used a finger prick in the mornings while on it, it was always in the 90s whereas usually its in the 80s.
The results were that empagliflozin did raise my average glucose by about ~4mg/dL, mostly by raising the low end/floor: my average on empagliflozin was 95.76 versus off at 91.95. Comparing the medians gave similar results, and as you might suspect, though, empagliflozin lowered the standard deviation a little bit, 9.70 compared to 11.27 normally. Interestingly, the highs, maximums and upper percentiles were almost identical. So it didn’t do anything to reduce spikes. So it seems to have prevented really low dips overnight, where most of my lower readings (in the 60s and 70s) occur.
To be thorough, I then performed a regression, adjusting for total daily calories and total daily carbohydrates (taken from my Chronometer app), just in case I was eating more while on empagliflozin. To my surprise, I was actually eating slightly more carbs off of it. The nutrition-adjusted efect was slightly larger than the unadjusted effect, about 4.65 mg/dL. Presumably this is due to a counteracting homeostatic effect, where my liver produces more glucose in response.
So for background, at the time I had been on 500mcg of semaglutide weekly and had been taking emiglimin daily, 1,000 mg, once at night also, about half the prescribed dose. These were unchanged though.
My question: are there any plausible benefits to taking something like SGLT2 inhibitors (or other drugs like imeglimin or acarbose) when your blood sugar is already really low? Another question is might these drugs be more effective for people on high carb diets? Right now, I am on a very high protein diet, 150mg to 200g daily out of my 3,000 calories, and usually about 100 grams of carbs. I realize this isn’t recommended by a lot of people, like Valter Longo, etc. But when I used to eat a lot of fruit and breads, my A1c would go up higher, albeit in ‘normal’ range, up to 5.4 for example. So now I’m thinking, perhaps you could get the best of both worlds, by eating healthy complex carbs, while also minimizing their negative effects by taking these drugs. What do you all think? I’ve since stopped taking empagliflozin, but might do an acarbose experiment next. But since my blood sugar is already very low, what biomarkers would I assess to see if they are having any benefit?
John, if I’ve learned anything from this thread, it’s that you need a robust insulin baseline to harness any longevity value from an SGLT-2 inhibitor. Taking it when your insulin is already depleted is a terrible ROI. Your insulin is the only thing keeping you out of ketosis. If that baseline is already near zero, adding an SGLT-2 inhibitor creates a massive, unbalanced risk. You are trading highly speculative, long-term longevity benefits for the immediate, real-world danger of DKA some have reported. When I receive my Jardiance, I will start with the baby dose, 5 mg. Since I am on OMAD (11th years) and Metformin, I will take it with meal and maintain my fluid balance by incorporating electrolytes i.e., sodium and potassium, throughout the day.
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Whole thread here about SGLT-2 inhibitors and their various benefits, independent or not of their blood sugar lowering abilities: Canagliflozin - Another Top Longevity Drug
Very useful to read. Very briefly :
- heart failure and cardiovascular protection
- kidney protection
- uric acid lowering
- anti inflammation and anti fibrotic effects
And more.
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A major clinically validated benefit is, perhaps the most critical for us on this forum: Klotho upregulation and preservation through both direct and indirect mechanisms. This is what motivates me to experiment with SGLT-2.
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You humble me. Do you think Jardiance helped you with (stubborn) fat loss?
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Hey Steve… I think my initial weight loss for muscle came with TRT for a year.
Then, I started rapamycin 6 mg weekly… -and after 3 months of weekly 6mg lost 25 pounds of visceral fat… just vanished. DEXA showed no fat there. Body used it.
Veins popped and I can eat non-stop
I think Jardiance is protecting me from my sugar and salt intake. Feeling great 
_
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Yes, but it has a double nature. An antioxidant in the blood, it can turn into an oxidant in the cells. High levels are linked to gout, inflammation, and worse.
I use febuxostat to keep my uric acid at 4.5. The stuff I get from India is legit.
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I took 12.5 mg Empagliflozin daily. I started losing weight each week. My body compensated with greater appetite. I switched to Dapagliflozin and this went away. My HBA1C did not change under either treatment. I have not had any noticeable side effects other than sometimes it burns when I pee. I assume there is some increased bacterial count accounting for this.
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