My uric acid was touching 7, After 1 spoon of Allulose daily it has dropped to 4.7.
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This is interesting. I’ll have to look into it. Thanks.
Well, I looked and it’s too good to be true. Compared to fructose and other sugars, which spike uric acid, allulose does nothing. It neither raises or lowers uric acid, at least at the somewhat modest doses of 25 g. At higher doses, however, allulose can induce a laxative effect. It is not a sugar alcohol, but it acts like one in the gut. When used as a sugar substitute, it can result in a transient reduction in uric acid, but that’s because of the reduction in sugar consumption.
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It makes really good ice cream. Inulin works good for ice cream too. Smooth.
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Oooh… I like this idea, Allulose and Inulin in ice cream. Its almost a health food at that point 
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Caution. A couple of years ago, I developed UTI and ended up in the hospital for surgical removal of a sebaceous cyst (abscess), along with continued antiobiotic use for a week. It was a minor surgery, however, I had to regularly visit the GP for about 10 times (over several weeks) for wound dressing post-surgery.
I attributed this to Empagliflozin (Jardiance) 10mg/day + Sirolimus 5mg once a week, which was my consistent protocol for 3-4 months or so, before the cyst (abscess) developed. My strong suspicion was that Empagliflozin caused elevated glucose in the urinary tract, and mTOR supression from Sirolimus attenuated my normal immune response, causing this serious infection. I couldn’t pin point to anything else. Since then, I swapped out Empagliflozin for metformin.
Although not everyone develps UTI from the SGLT2/flozins (perhaps, it is dependent on dosage and individual susceptibility), I’m leaning to think that the susceptibility can be more pronounced when combined with rapa.
If you do happen to be on this combo (SGLT2 + rapa), especially DIY, please ensure you don’t ignore any subtle/obvious symptoms (UTI or related). If you do encounter infection symptoms, then you may want to start antibiotics immediately.
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Thanks for posting. Very sorry to hear of your experience with the UTI, but thanks for the cautionary note. We need to hear these as well as the successes.
Was that the only time you’ve ever had a UTI?
I’m wondering if there are any predisposing factors that might influence whether someone gets them. The biggest outlier seems to be being female vs. male (about 30X higher for females it seems). I wonder also if there are certain types of diet more predisposing (e.g higher carb , more sugar more risk?, a friend who is a pharmacist told me the higher sugar in the urine , from the SLGT2 is likely the promoter of bacteria in the UT.). My point here is, is there anything we can control to change our risk of UTI?
I’ve been taking empagliflozin for a few years now, off and on, and no issues. But I also know that UTIs are more common with SGLT2 inhibitors.
Here is the list of early signs and symptoms of UTIs - its good to keep them in mind when trying the SGLT2 inhibitors.
Symptom Classification: Obvious vs. Subtle Presentations
The clinical manifestations of UTIs are categorized by anatomical involvement and the clarity of their presentation.
| Anatomic Site / Condition | Obvious (Classic) Symptoms | Subtle / Atypical Symptoms |
|---|---|---|
| Lower Urinary Tract (Cystitis) | * Dysuria (burning or sharp pain during micturition) * Urinary frequency and urgency * Suprapubic tenderness * Gross hematuria (visible blood, cola-colored, or bright pink urine) | * Vague lower abdominal pressure or fullness * Isolated malodorous or cloudy urine (frequently secondary to dehydration or diet rather than active infection) |
| Upper Urinary Tract (Pyelonephritis) | * Unilateral or bilateral flank pain * Costovertebral angle (CVA) tenderness * High-grade pyrexia (fever) with rigors/chills * Nausea and emesis (vomiting) | * Generalized malaise or profound fatigue * Epigastric or diffuse abdominal pain mimicking an acute abdomen * Hypotension without clear localization |
| Prostate (Acute/Chronic Bacterial Prostatitis) | * Perineal, penile, or pelvic pain * Obstructive voiding symptoms (hesitancy, weak stream, acute urinary retention) * Painful ejaculation | * Dull low back pain * Recurrent, unexplained lower urinary tract symptoms without systemic febrile indicators |
| Urethra (Urethritis) | * Mucopurulent or clear urethral discharge * Severe localized burning during initial voiding phase | * Isolated urethral pruritus (itching) * Mild meatal erythema (redness) |
Predisposing Risk Factors for UTIs
The incidence and prevalence of urinary tract infections (UTIs) are highly stratified across different demographics. Susceptibility is determined by anatomical structures, physiological states, and metabolic profiles.
Sex-Based Disparities (Anatomical Architecture)
Biological sex is the most profound determinant of UTI frequency. Adult females experience a lifetime incidence of 50% to 60%, contracting UTIs up to 30 times more frequently than adult males under the age of 50.
According to data compiled by the Centers for Disease Control and Prevention, this disparity is driven by clear anatomical factors:
-
Urethral Length: The female urethra is significantly shorter (approximately 4 cm) than the male urethra (approximately 20 cm). This minimizes the physical distance uropathogens must ascend to colonize the bladder.
-
Anatomic Proximity: The female urethral meatus sits in close proximity to both the vagina and the anus. The perianal region acts as the primary reservoir for uropathogenic Escherichia coli (UPEC), facilitating mechanical translocation during sexual activity or standard hygiene practices.
In contrast, young and middle-aged males are highly protected by a long urethra, prostatic antibacterial secretions (zinc-dense fluids), and a greater distance between the meatus and the anus. Consequently, any UTI documented in an adult male is clinically categorized as a complicated UTI, requiring investigations into structural abnormalities or prostatic involvement.
Body Mass Index and Adiposity (Metabolic and Cellular Drivers)
Epidemiological cohorts demonstrate a distinct correlation between elevated Body Mass Index (BMI) and UTI risk, while underweight status presents a different clinical profile.
Overweight and Obese Populations (BMI greater than 25)
Data published via PubMed / PMC indicates that individuals with obesity (BMI greater than 30) have a significantly higher relative risk of developing both simple cystitis and severe pyelonephritis. The underlying pathology involves three distinct mechanisms:
- Mechanical and Hygiene Constraints: Increased adipose tissue in the pelvic and perineal areas creates deep skin folds that retain moisture and alter local dermal heat. This microenvironment accelerates the proliferation of Gram-negative rods. Physical mobility limitations can also impede ideal perineal hygiene.
- Metabolic Synergies (Glycosuria): Obesity strongly correlates with insulin resistance and Type 2 Diabetes. Elevated systemic glucose often leads to glycosuria (glucose excretion in the urine). This provides a nutrient-dense substrate that accelerates bacterial replication within the lumen of the bladder.
- Urothelial Cellular Alterations: Recent transcriptomic models reveal that obesity elicits clear changes in bladder urothelial gene expression. It upregulates focal adhesion kinase (FAK) signaling pathways, which morphologically alters the bladder lining and directly promotes UPEC cellular invasion into host cells.
Underweight Populations (BMI less than 18.5)
An underweight BMI is not an independent risk factor for UTIs in the general population. However, a significant correlation emerges if low BMI is a secondary consequence of severe protein-energy malnutrition, advanced age-related cachexia, or uncontrolled eating disorders. In these specific sub-populations, the mechanism is systemic immune suppression—specifically a decline in cell-mediated immunity and a thinning of mucosal barrier protections.
Age and Hormonal Disparities Across the Lifespan
Disparities shift dynamically as populations age, dictated primarily by hormonal transitions and structural senescence, as outlined by the Urology Care Foundation.
[Youth] Females slightly lead → [Adulthood] Female spike (30:1 ratio) → [Geriatric] Gap narrows due to BPH & Estrogen loss`
- Postmenopausal Females: The cessation of ovarian estrogen production causes structural atrophy of the urogenital tissue. Crucially, it depletes glycogen stores within the vaginal mucosa. This causes a dramatic loss of protective Lactobacillus species, raising vaginal pH from an acidic 4.5 to a neutral or alkaline level. The loss of this acidic shield allows rapid colonization by pathogenic Enterobacteriaceae.
- Aging Males: Beyond the age of 65, the incidence gap between sexes narrows significantly. This is primarily caused by the near-ubiquitous development of Benign Prostatic Hyperplasia (BPH). As the prostate enlarges, it compresses the prostatic urethra, causing bladder outlet obstruction. The resulting urinary stasis and elevated post-void residual (PVR) volumes create an ideal environment for bacterial colonization.
Scholarly Debates and Knowledge Gaps
A current debate in urological epidemiology centers on whether obesity acts as a completely independent risk factor for UTIs, or if it is merely a confounding proxy for subclinical glucose intolerance and altered pelvic floor mechanics. Longitudinal datasets are currently insufficient to prove whether targeted adipose reduction directly downregulates inflammatory signaling cascades (like FAK activation) in human bladder tissues independent of changes in systemic glycemic control.
Dietary impact on Risk for UTI:
While dietary patterns are not considered independent primary causes of urinary tract infections (UTIs), diet plays a critical regulatory role in modulating the urinary microenvironment. Specific foods, macronutrients, and fluid volumes alter urinary pH, host immunity proteins, and gut microbiome metabolites, which directly impacts the colonization kinetics of uropathogenic bacteria.
Dietary composition directly alters the baseline reservoir of pathogens within the gastrointestinal tract. A large, 9-year prospective cohort study published in Scientific Reports observed that individuals following a vegetarian dietary pattern experienced a 16% relative risk reduction in UTIs compared to non-vegetarians.
The mechanism driving this disparity involves Extraintestinal Pathogenic Escherichia coli (ExPEC) , the specific bacterial strains responsible for roughly 65% to 75% of all UTIs. Commercial poultry and pork act as natural zoonotic reservoirs for these ExPEC strains. Regular consumption of contaminated meat allows these strains to colonize the human intestinal tract. Once established in the gut microbiome, they can easily translocate across the perineum and ascend into the lower urinary tract. By avoiding these meat reservoirs, plant-based diets limit intestinal colonization by highly virulent uropathogenic strains.
3. Dietary vs. Supplemental Anti-Adherence Substrates
Certain dietary components possess specific anti-adherence properties that prevent bacteria from attaching to the bladder wall.
The diagram below outlines how specific plant compounds interfere with the structural mechanisms uropathogens use to anchor themselves to the urinary tract lining.
- Proanthocyanidins (PACs): Found predominantly in cranberries, A-type PACs physically bind to the external P-fimbriae (hair-like appendages) of E. coli. This binding prevents the uropathogen from latching onto the uroepithelial lining, allowing the bacterial cells to be washed away during urination.
- D-Mannose: This simple sugar matches the configuration of the receptors on bladder cells. When present in the urine, it acts as a competitive inhibitor, binding to the FimH adhesins on the bacteria so they cannot stick to the bladder.
The Dosing Disconnect
A critical diagnostic and therapeutic knowledge gap exists regarding the distinction between dietary intake and supplemental dosing. A clinical pilot study published in the EMJ Urology evaluated postmenopausal women with recurrent UTIs and found no statistically significant link between natural dietary intake of D-mannose-containing fruits and a reduction in UTI risk.
The quantities of active anti-adherence compounds obtained through standard dietary consumption of fruits and unrefined juices are typically far lower than the standardized, highly concentrated thresholds required to exert a therapeutic anti-adherence effect in vivo.
4. Hydration Volumetric Kinetics
Volumetric fluid intake remains the most robustly validated dietary intervention for reducing infection risk. A landmark randomized controlled trial published in JAMA Internal Medicine tracking women with recurrent cystitis who habitually consumed less than 1.5 liters of fluid per day demonstrated that increasing daily water intake by an additional 1.5 liters reduced recurrent UTI episodes by 48%.
| Metric | Low Fluid Cohort (Baseline) | Increased Hydration Cohort (+1.5L/day) |
|---|---|---|
| Mean Annual UTI Episodes | 3.2 episodes | 1.7 episodes |
| Antibiotic Regimens Required | 3.6 courses | 1.9 courses |
The underlying mechanism is mechanical shear stress. Increased fluid throughput dilutes the concentration of nutrients available to bacteria in the bladder and ensures frequent, high-volume voiding. This repeatedly flushes out unattached planktonic bacteria before they can complete the complex process of cellular adhesion and intracellular invasion.
Scholarly Debates and Knowledge Gaps
The primary conflict in current urological nutrition research centers on the optimal manipulation of urinary pH. While historical protocols relied on mega-doses of Ascorbic Acid (Vitamin C) to intentionally acidify the urine to exert a bacteriostatic effect, contemporary discovery of the siderocalin-iron sequestration pathway implies that an alkaline or neutral urine pH (achieved via diets rich in fruits and vegetables or supplemental potassium citrate) actually optimizes native immune defenses.
Longitudinal human data is currently lacking to prove whether altering the diet to explicitly pair high-polyphenol intake with alkalizing agents can reliably achieve clinical efficacy equivalent to low-dose antibiotic prophylaxis for recurrent UTIs.
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@RapAdmin, that was not very good in the particular context brought up by the poster. It was not helpful.
Here’s what needed asking: what factors are involved in SGLT2i associated UTIs - because this is a distinct subcategory, and directly relevant to the poster’s experience.
There are studies directly addressing this question. I am not going to cite them here, because I want to give your LLM AI that you pay for a chance to shine 
. If there are any significant omissions, I might come back and point them out, if only to grind my anti-AI axe a bit 
.
But joking aside, this is worth addressing head on, as I’m sure others may be interested in the subject. TIA! 
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On the sebaceous cyst issue. Some clarity here because sebaceous cysts typically have absolutely nothing to do with UTIs.
A sebaceous cyst is initially and usually not infected. They are very common and are basically a sweat gland that gets trapped under the skin and overtime builds us a cheesy substance in a lined cavity. (This is my attempt at layman definition). The back is the most common place.
This often persists for years until they are annoying enough to remove or they become infected. Once infected, they become symptomatic beyond cosmesis. They almost never require hospitalization and frequently respond to antibiotics alone but I&D is frequently helpful. We don’t generally refer to that as surgery. Excision of cysts are often done but usually after the acute infection.
They are in no way associated with the urinary tract. They are from skin. Now, if you get bacteremic from a UTI, then that could potentially infect the cyst although this is not generally something that happens. If you are bacteremic, this is a non serious outcome but there are much worse outcomes.
Now, another option is what I might call the distracted immune system where a cyst with a few bacteria living there is allowed to flourish when the body is sick fighting a UTI. Unrelated to bacteremia. We are this with surgery where people get unrelated infections in the first week after the procedure.
Last option is a mis labeling of a Bartholin’s cyst as a sebaceous cyst. These are still different but more closely related. These cysts are just inside the vaginal wall.
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I don’t know where you have read the horror stories since the very first horror one I ever read is your story. That is not to say there aren’t any, but at least I haven’t read/seen one yet.
I have been on 12.5mg EMPA for past two years with no side effects that I can tell, and not much change on FG either. My HA1C is stubborn at 5.2 and has been there pre and after Empa. I also do Metformin 1000mg DR and acarbose with main meal and my FG moved from around 105 to mid 90’s. I’m really surprised that my FG and Ha1c haven’t moved much with all these diabetes drugs I’m taking, good news though is that I’m not diabetic nor pre-diabetic and never was. Because If I were I am not responding much to these drugs, so I’d have to look for something different.
Most of us do antibiotics the day we take rapa, so no need to wait for infection. The day of my rapa i take 100mg doxy and same the next day, then I take 25-50mg daily after. Never had an infection problem since I started this regimen.
Oh I see. I never took antibiotics preventatively. Just curious, do you have any general concerns about impact on microbiome long term?
not at low doses. apparently, there is some people on these boards that haver been taking doxy 100mg for last 20 years and they said they’ve had no issues. I myself take it only two days at 100mg, then at 25-50mg which is considered sub antibacterial. Actually I’ve only been doing it this way continuously for last three months, but I used to take it 100mg with Rappa for last 3 years on and off and. so far nothing good or bad that I can tell other than no infection of any kind. BTW, I consume a lot of cultured/butter milk and that is believed to help with gut microbiome. Yogurt and kefir are also good but don’t like the taste of either, and really like the taste and texture of buttermilk, plus it is easy to make my own. When I’m about 80% through the container, I just fill it with organic milk, mix it a bit, and leave it out of fridge for 10-12 hours. Walla, perfect buttermilk/kefir in never ending supply LOL.
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Thanks for sharing your comments. Well, in my specific case of infection (which was a one-off occurance 2 years ago), the GPs and the clinician at the hospital used all these terms interchageably (sebaceous cyst, abscess and UTI), although I’m not sure what could have led to what. I had symptoms of UTI, along with presence of cyst, infection that was dominant in the pelvic region, however, it was systemic as well (feverish symptoms on a persistent basis for about a couple of weeks).
I have been on rapa for about 2.5 yrs now (been taking it cyclically). Except for very mild ulcers (which only occured a couple of times in my early days of staring on rapa), I never faced any issues… except during that one-off phase 2 yrs ago when I added empagliflozin. It wasn’t a coincidence at all, it was quite obvious to me that my body doesn’t do well when empagliflozin + rapa is taken together.
My A1C toggles between 5.4 to 5.7%, which I’m keen to optimize. It appears there is a strong case that SGLT2i is more effective and more promising that metformin, and has benefits beyond glucose control.
At some stage in the future, I’ll re-experiment adding back empagliflozin (perhaps when I’m cyclically off rapa), titrating carefully and see how it works out.
I’ll also analyse notes from @RapAdmin above.
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Is this accurate (most people)? I am not challenging - genuinely new to this. I have some antibiotics stored away, but was not taking anything weekly.
I don’t think thats accurate at all - I think it’s only a small percent of people who take rapamycin who also take doxycycline. I think a small micro-trend might have started in this area when Peter Diamandis started doing it a few years ago (I think he’s now stopped): Peter Diamandis Longevity Protocol: Weekly 6mg Rapamycin + 100 mg Doxycycline
I do keep doxy on hand just in case I get an infection, but I’ve only used it once in 6 years of rapamycin dosing.
I believe one of the issues with frequent dosing of doxy or any other antibiotic is this: One course of antibiotics can change your gut microbiome for years (New Scientist)
Personally, I wouldn’t do it.
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Meant to use “some” of us not most. I only know 4 of us already and four is definitely not most LOL. I’m sort of intrigued though by Doxy, especially at sub antibacterial doses. There is some literature on its benefits, and I believe one of our docs (at least) on here has supported it.
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I am Microdosing terzepatide. I am planning to titrate up to 1.25 if no issues arise and am at .75 currently. Normal Starter dose is 2.5. My understanding is that bone remodeling occurs overwhelminging as a consequence of weight loss and I don’t plan to lose much weight. I have already seen a meaningful effect on my glucose and am taking it for Long Covid as well as cardiovascular effects secondary to glucose. I am using a CGM to monitor the glucose effect. I have read it is the length of time at higher values (some use 140 or above) that have negative cardiovascular effects and that a CGM is the way to look for those spikes. My HbA1c is below pre diabetic. My genetics predisposes me to spikes.
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I recommend checking the CGM readings with a finger prick glucose meter. In my experience the CGMs can be pretty far off the mark.
It actually gave me systems of worse than long covid LOL, I understand the lowering of glucose part but maybe not the best idea for long covid.