This doesn’t happen as much as people seem to think it does
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It’s always been the thing that has held me back from taking it. I’m going to give it a try.
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My experience, maybe more frequent for a couple days, then normalizes.
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I never noticed any frequency at all. My UA had 3+ glucose so it is working.
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If you eat a lot of cookies/cakes etc (like I do) you will not urinate any more often (surprise!). But it takes Sodium to eliminate glucose. Sodium really really seems to drop in my N=1. You may find yourself generally weaker if you don’t take a high sodium electrolyte supplement like LMNT or equivalent, a few times/week depending on your chocolate intake! I find SGLT2i an amazing, zero side effect, medication for myself. I cannot tolerate GLPa and I find that my weight and appetite is well moderated with Empagliflozin.,
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SGL2i’s do not affect sodium excretion.
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A relevant 20-minute Podcast about Kidney Aging and treatment for that:
Core issues:
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kidney function declines past age 35 and increases in speed past age 70
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decreased kidney function in an elderly is functionally not different than kidney failure in a younger person
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elderly people have only a few years lifespan left; therefore it’s best to manage symptoms (i.e. cardiovascular problems) and avoid kidney stress (e.g. not taking medications that need to be excreted by the kidney
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if a 85 year old is very fit and it’s according to his lifestyle plans, he can be started on SGLT2i or ACE/ARB after kidney failure is imminent
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most 85 year olds should not get treated due general frailty and little remaining lifespan
It’s funny of course, that SGLT2i and ARBs specifically prevent kidney function decline in the first place (above and beyond blood pressure effects) and for almost all have little to no side effects. You may come to the conclusion to start at age 35 instead of waiting till functional CKD in the elderly. Unless you’re living according to " yeah I’m dead at 80, so I don’t give a f*** ".
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I started Jardiance 12.5mg twice but I had to stop after a few weeks as it makes me very tired after working out.
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I’ll go out on a limb and mention something no one else talks about 
I didn’t notice any more frequency, but I do notice the effect it has on my toilet bowl.
“SGLT2 inhibitors work by dumping glucose into urine — roughly 50–80g/day. That’s a couple tablespoons of sugar going into the bowl daily, which feeds yeast, mold, and bacterial biofilm in standing water” from Opus.
I notice this within only a few days, and my toilet needs to be cleaned more often than my past routine of once per week.
When I first saw this I worried something was wrong with me!! I have since discovered it happens to plenty of people, but obviously not all. I get incredibly high glucose spikes, so Opus explained I’m probably dumping out more sugar and that is why my effect might be greater than the average person. Who knows!
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Oh for sure! I noticed this as well.
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Just a re-assuring comment on a study linked in another sub:
the authors take a very differentiated look at patient data by various sub-categories. Core results relevant for “normal” healthy people:
the relative slow-down of kidney function decline was independent of baseline eGFR and baseline albuminera (protein in urin - a measure of kidney disfunction)
So even folks with still borderline normal eGFR and low protein in urin - that is, people with generally still relatively healthy kidneys and no acutely damaging processes - had a similar percentage of reduced decline in kidney function as people with end-stage kidney disease. The absolute reduction in decline was lower than in people with severe CKD - simply because the placebo-group in severe CKD has a large absolute drop in kidney function. Where as the placebo-group in still normal kidneys had a low absolute drop. Note: this effect is independent of diabetes status.
All this re-affirms the assumption, that regular healthy people could start SGLT2i at a young age to protect against aging related decline in kidney function.
A more detailed comment of this study:
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A. I have noticed nothing since taking empagliflozin. Since I take Imeglimin for my primary glucose control, I don’t see very much effect when I add empagliflozin.
B. I do see a drop in my eGFR readings. Gemini Pro assures me that this is expected and a good thing because it shows the empagliflozin is working.
Gemini’s explanation
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I think one way of teasing out the MOA of flozins in kidney protection is to combine a flozin with another kidney impacting agent, like an ARB and watching what happens - might illuminate pathways. I posted some studies to that effect in another thread, but it is also of independent interest, because many on this site already combine several drugs which have kidney impact. We have to be careful to make sure that while each drug might be kidney beneficial on its own that it doesn’t interfere or get in the way of another drug achieving overall a less optimal effect. The papers I posted dealt with ARBs and flozins. FWIW, I take both empagliflozin (25mg/day) and telmisartan (80mg/day), plus drugs which are orthogonal to the kidney like pitavastatin. Of course then there is rapamycin which is a whole other ball of wax when it comes to the kidney - really wonder about DDI on that one.
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I got a UTI too when I was on dapa. My anatomy since birthing 5 kids has made me prone to them so I’m skipping dapa for the foreseeable future.
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The way to go if I were dead set on continuing and if anyone was on the fence just due to the UTI risk would be to add D-mannose as a supplement in significant amounts (say, 2 g in the am, 2 g in the PM). I think theoretically it should slash the risk of UTIs but my pill burden is too high right now for another thing.
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I tried Jardiance about a year ago. 10mg daily. In addition to rapa, I also take carvedilol, ezetimibe, atorvastatin, losartan, and tadalifil. I’m not diabetic or prediabetic, my A1c is around 5.1. My diet is generally low carb.
My experience with Jardiance was negative. I had a constant need to pee, and I developed UTIs. As for the risk factors, I am not female or overweight, but I likely have a degree of BPH - even without being on Jardiance I have a degree of PVR that’s annoying. Possible that I wasn’t drinking enough water at the time.
It’s a real dilemma because I can see the benefits of Jardiance but didn’t like the UTIs. Looking for ways to mitigate.
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Mitigate? I just dropped it, D-mannose as a preventative. Look into it. I just can’t handle more pills at the moment but it works.
I have not had any issues using empaglifozin for 3 or 4 years now. But I’m interested in this topic - so did a query on D-mannose as preventative of UTIs. Here is the response from Gemini Pro Extended (Paid).
Prompt:
Role: Urologist. Task: Identify and summarize the clinical evidence that D-mannose is a preventative for UTIs.
Clinical Bottom Line
D-mannose should not be recommended as a standalone prophylactic agent to prevent recurrent urinary tract infections (rUTIs). Despite a plausible in vitro mechanism and early low-quality trials suggesting efficacy, the most rigorous randomized controlled trials (RCTs) to date demonstrate that daily D-mannose is clinically indistinguishable from placebo for preventing UTI recurrence in women. Consequently, major urological guidelines have been updated to explicitly advise against its use for this indication.
Theoretical Mechanism of Action vs. Clinical Reality
D-mannose is an aldohexose sugar that is rapidly absorbed and excreted in the urine. The theoretical basis for its use relies on competitive inhibition. Uropathogenic Escherichia coli (UPEC) utilize type 1 pili equipped with FimH adhesins to bind to mannosylated uroplakin proteins on the uroepithelium. In vitro, exogenous D-mannose saturates these FimH adhesins, preventing bacterial adhesion and allowing the pathogens to be flushed out during micturition.
While this pharmacological mechanism is biologically plausible and demonstrated in animal models (informed speculation), it consistently fails to translate into clinically significant infection prevention in human trials (verified fact).
Evolution of the Clinical Evidence
The scholarly debate regarding D-mannose has been heavily skewed by publication bias and poor study design in earlier literature.
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Early, Low-Quality Data (Pre-2024): Prior to 2024, the clinical rationale for D-mannose relied heavily on small, open-label, single-center trials. The most cited study (Kranjčec et al., 2014) reported a striking drop in UTI recurrence (15% for D-mannose vs. 61% for no prophylaxis). However, utilizing “no prophylaxis” rather than a placebo control severely confounded the data, as the requisite hydration to ingest the powder could entirely account for the urinary flush effect. A 2022 Cochrane Review accurately noted that the existing evidence was of very low certainty and insufficient to confirm efficacy.
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Definitive High-Quality Data (2024): The clinical paradigm shifted decisively with the publication of the MERIT trial (Hayward et al., 2024, JAMA Internal Medicine). This multi-center, double-blind, placebo-controlled RCT (N=598 women) rigorously tested 2g of daily D-mannose over six months. The trial found no statistically significant difference in UTI recurrence (51.0% in the D-mannose arm vs. 55.7% in the placebo arm; RR 0.92, 95% CI 0.80–1.05). Secondary outcomes, including antibiotic usage and time to next infection, were identically null.
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Recent Meta-Analyses (2025): A subsequent systematic review and meta-analysis aggregating 6 RCTs (N=1,167) confirmed the MERIT findings, showing no reduction in recurrent UTIs compared with placebo or standard antibiotics (RR: 0.57, 95% CI 0.29–1.15; p<0.01).
Current Guideline Consensus & Longevity Implications
Reflecting this updated evidence, the American Urological Association (AUA), Canadian Urological Association (CUA), and Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction (SUFU) amended their joint rUTI guidelines in late 2025. The amendment formally recommends against the use of D-mannose alone for UTI prevention.
For longevity and healthspan optimization, abandoning ineffective prophylactics is critical. Relying on failed preventative measures like D-mannose increases the incidence of active infections, thereby necessitating recurrent systemic antibiotic exposure. Repeated antibiotic use induces microbiome dysbiosis—a verified driver of systemic inflammation, immune dysfunction, and accelerated cellular aging. Clinicians should pivot to evidence-backed non-antibiotic prophylaxis, such as vaginal estrogen (in postmenopausal women) or methenamine hippurate.
and then another query on what does work for UTI prevention:
Clinical Bottom Line
The clinical paradigm for recurrent urinary tract infection (rUTI) prophylaxis has shifted decisively away from continuous low-dose antibiotics toward antimicrobial stewardship and barrier protection. The 2025 American Urological Association (AUA) and European Association of Urology (EAU) guidelines formally endorse several non-antibiotic agents. For optimizing healthspan and longevity, replacing chronic antibiotics with proven preventative compounds is critical to prevent microbiome dysbiosis, systemic inflammation, and subsequent metabolic disruption.
Guideline-Endorsed Preventative Compounds
Methenamine Hippurate
- Mechanism of Action: A synthetic salt that hydrolyzes in acidic urine (pH < 5.5) to form formaldehyde, a non-specific bactericidal and bacteriostatic agent. Because it acts universally as a localized urinary antiseptic rather than a targeted systemic antibiotic, it does not induce antimicrobial resistance or alter the gut microbiome.
- Clinical Evidence: The rigorous ALTAR Trial (N=240 women) definitively established non-inferiority against continuous daily antibiotics (nitrofurantoin, trimethoprim, or cefalexin) over 12 months. The incidence was 1.38 UTI/year for methenamine vs. 0.89 for antibiotics—a clinically negligible absolute difference of 0.49 that easily met the non-inferiority margin.
- Status: Formally recommended in the updated 2025 AUA rUTI Guidelines as a primary non-antibiotic prophylactic option.
Cranberry Proanthocyanidins (PACs)
- Mechanism of Action: Type-A proanthocyanidins competitively inhibit P-fimbriae and type 1 fimbriae of uropathogenic Escherichia coli (UPEC), preventing adhesion to uroplakin receptors on the bladder epithelium.
- Clinical Evidence: Historically debated due to poor trial standardization, a massive 2023 Cochrane Systematic Review of 50 RCTs (N=8,857) conclusively demonstrated that cranberry products significantly reduce UTI incidence in women with recurrent infections and in children.
- Status: The 2025 AUA guidelines now officially advise offering cranberry prophylaxis. Crucial Caveat: Efficacy is highly dose-dependent; generic juices are insufficient. Clinical efficacy requires a daily dose of at least 36 mg of standardized, soluble PACs.
Vaginal Estrogen (For Perimenopausal/Postmenopausal Women)
- Mechanism of Action: Systemic estrogen depletion causes urogenital atrophy and a rise in vaginal pH, wiping out protective Lactobacillus species and permitting colonization by enteric coliforms. Topical estrogen restores the glycogen-rich mucosal epithelium, allowing Lactobacilli to thrive, lower the pH, and competitively exclude UPEC.
- Clinical Evidence: Robust and undisputed. Topical vaginal estrogen drastically reduces rUTI rates compared to placebo without systemic absorption risks.
- Status: Universally endorsed as foundational therapy by both AUA and EAU for estrogen-deficient women.
Emerging Phytotherapeutics (2025 EAU Updates)
The 2025 EAU Guidelines on Urological Infections highlight several emerging nutraceutical complexes that demonstrate clinical promise, marking a shift toward phytotherapeutics in European urology:
- Xyloglucan, Hibiscus, and Propolis: This combination acts as a mechanical mucoprotectant. A recent meta-analysis of 178 patients confirmed its ability to reduce rUTI risk versus placebo by creating an inert barrier that prevents UPEC adhesion to the uroepithelium.
- Centaurii herba, Levistici radix, and Rosmarini folium: This standardized herbal triad has demonstrated non-inferiority to single-dose fosfomycin trometamol for acute uncomplicated cystitis and shows promise in reducing long-term recurrence rates.
Longevity & Healthspan Implications
Chronic antibiotic administration—the former gold standard for rUTIs—is fundamentally incompatible with longevity protocols. Broad-spectrum antibiotics decimate the gut microbiome, halting the production of critical short-chain fatty acids (like butyrate) and anti-aging metabolites (such as Urolithin A, which requires a healthy gut flora to synthesize from dietary ellagitannins). This dysbiosis drives intestinal hyperpermeability, endotoxemia, and systemic “inflammaging.” By transitioning to methenamine hippurate or targeted PACs, patients preserve their microbial diversity while effectively controlling pathogen colonization.
Knowledge Gaps & Required Data
- Microbiome Resiliency Profiling: We lack granular, longitudinal data detailing exactly how rapidly the gut and uro-microbiomes recover following a transition from continuous prophylactic antibiotics to localized antiseptics like methenamine.
- Standardization of Nutraceuticals: The EAU specifically notes significant heterogeneity in phytotherapeutic trials. Strict pharmacokinetic data, standardized extraction protocols, and certified certificates of analysis (COAs) for active compounds like xyloglucan and specific Lactobacillus strains are required before these achieve the same universal clinical consensus as estrogen or methenamine.
Prevention of Recurrent UTI Using Natural Therapies with Dr. Brian Flynn This presentation is highly relevant as a clinical urologist explicitly details the mechanisms, exact dosing requirements (36 mg PACs), and guideline-based evidence for non-antibiotic UTI prevention strategies including cranberry, methenamine, and vaginal estrogen.
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Follow-on Prompt:
What cranberry juices have the validated levels of Cranberry Proanthocyanidins (PACs) to help protect against UTIs, and what dose daily is recommended in this role?
The Clinical Dose
The clinically validated, guideline-recommended daily dose for UTI prophylaxis is 36 mg of soluble, A-type Proanthocyanidins (PACs) .
The Reality of Cranberry Juice
To be direct: No commercial cranberry juice provides validated, standardized levels of PACs. Attempting to achieve clinical UTI prophylaxis through juice is an unreliable and metabolically detrimental strategy for several reasons:
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Shelf-Life Degradation: Soluble PACs are highly unstable in liquid suspension. While 8 to 10 ounces of a 27% cranberry juice cocktail may theoretically contain 36 to 41 mg of PACs at the time of pressing and bottling, these compounds actively degrade the longer the bottle sits on a store shelf.
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Zero Standardization: Commercial juice manufacturers do not measure, standardize, or guarantee PAC concentrations on their labels. The PAC yield varies wildly based on harvest conditions, pressing techniques, and dilution.
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Metabolic Toxicity: To hypothetically reach the 36 mg PAC threshold using standard cranberry juice cocktail requires consuming high amounts of liquid laced with refined sugars. This causes acute glycemic spikes, drives insulin resistance, and fundamentally conflicts with any longevity or healthspan protocol. While 100% pure, unsweetened cranberry juice lacks the sugar payload, it remains unstandardized for PACs and its extreme astringency severely limits daily patient compliance.
The Clinical Alternative: Standardized Extracts
Because juices cannot guarantee the required dosage, clinical urology relies on standardized cranberry extract supplements. To be effective, a supplement must be third-party tested using the BL-DMAC method (the scientific standard for quantifying soluble A-type PACs) to guarantee exactly 36 mg per dose.
The three primary brands heavily utilized in clinical practice that independently certify this 36 mg DMAC-verified threshold are:
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ellura : Utilizes a highly concentrated juice extract.
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TheraCran One : An NSF-certified whole-cranberry extract providing both soluble and insoluble PACs.
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Utiva UTI Control : A high-potency extract utilizing 240 mg of raw material to yield the 36 mg PAC standard.
If you are incorporating this into a longevity-focused preventative stack, bypass the juice entirely and utilize a DMAC-verified 36 mg extract capsule.
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I too have not had any issues with empagliflozin in the roughly two years of use (25mg/day). That said I also consume a morning drink, first thing after waking up, which contains cranberry extract powder among other things dissolved in about 2 cups of green tea. It’s about 2 teaspoons of the powder, for sure much in excess of 3-4g, which might or might not be enough for UTI prevention, but quite frankly if that happens, it’s an incidental benefit as I take it for general cranberry polyphenol benefits (CV etc.).
But about once a month I also test my urine with a strip, just to make sure I don’t have some occult urogenitary infection I’m unaware of. So far, so good. For me, empagliflozin has been a complication free drug. YMMV.
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