Hello fellow longevity seeking guys and gals! For those of you taking Arcabose, I wanted to give you a heads up about something that happened to me recently. I went to see my urologist because I’ve been suffering for years from frequent urination particularly at night. He did a routine urinalysis and my glucose came back at 1000 (it’s supposed to be zero!). He didn’t know I was taking Arcabose and explained that it was the reason the glucose was so high (because I’m not diabetic). He said this is certainly exacerbating my nocturia. I was taking a pretty high dose (200 mg with my evening meal).

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I didn’t know acarbose did that. It sounds like SGLT2 drugs like Farxiga.

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That’s not a thing you see with acarbose. Think about it’s mechanism: it prevents carbohydrates from being absorbed in the intestine. This would (and does) result in some bothersome side effects coming out the end of the intestine in the form of diarrhea and flatulence.

The diabetes drugs associated with high glucose in your urine are called SGLT2 inhibitors. These specifically work in the kidney to prevent the reabsorption of glucose into the blood stream, lowering blood glucose but raising urinary glucose as part of how they work.

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Good point. I also take Empagliflozin, could it be that?

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100% yes. It’s the empagliflozin causing the high glucose in your urine. Stop that, continue with the acarbose.

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Try a Google search for “Fournier gangrene SGLT2” and see what can happen when taking drugs like empagliflozin. Don’t click on the images tab if you’re queasy.

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Why stop? It sounds like the drug is working to get rid of the glucose.

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Because of the frequent nightly urination disrupting his sleep. Which is more important for longevity; an SGLT2 inhibitor in a non-diabetic already on acarbose or improved sleep for the rest of his life?

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I see. Why wasn’t the acarbose blocking the carb uptake?

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Acarbose doesn’t block 100% of all carbohydrates from the diet. It will lower blood glucose by blocking a portion of them.

Our liver also supplies the body with glucose to keep blood glucose in a range and prevent hypoglycemia.

The glucose in the blood is what’s being filtered through the kidneys and typically reabsorbed into the bloodstream, but that step is blocked with the SGLT2 inhibitor leading to the glycosuria and increases the frequency of urination.

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So, it’s pick your poison time: high blood glucose or bad sleep (which will give you high blood glucose)? Maybe a third option is called for in this situation. I take metformin.

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Yes - its now the SGLT2 inhibitors work, you pee out the sugar instead of digesting it. Its also why the risk of urinary tract infections is higher; because bacteria in the urinary tract love sugar and can really increase in number (for some people, in some situations).

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Stopping the SGLT2, unless your diabetic will not cause high blood glucose. It isn’t necessarily the SGLT2 that is causing your nocturia. Stop it and see what happens. And, I’ve never seen Fournier’s gangrene in a non diabetic.

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All true, but how many patients do you see taking SGLT2 inhibitors that aren’t diabetic? That number, close to zero I would imagine, is a possible reason why you haven’t seen Fourniers gangrene in a non-diabetic.

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You are correct. Patient count of zero. But to say that Fournier’s would happen in a SGLT2 user would imply that glucosuria is the cause which I don’t think is true.
Btw, although I’ve never seen it, Fournier’s does happen in non diabetics.

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Really? You’re concerned if 13 people out of 135,000 get a side effect? I can’t imagine I’d leave the house much if I was afraid of hazard ratios like that.

Among 138,158 SGLT-2 inhibitor users, there were 13 cases of hospitalization for Fournier gangrene (unadjusted incidence rate, 15.0 per 100 000 person-years) compared with 24 cases (unadjusted incidence rate, 9.7 per 100 000 person-years) among 360 685 DPP-4 inhibitor users, corresponding to an adjusted rate difference of 6.7 excess hospitalizations per 100 000 person-years (95% CI, –2.8 to 16.1 per 100 000 person-years) and an adjusted hazard ratio of 1.73 (95% CI, 0.87-3.42) (Table 2).

Seriously - this is in a sample of largely obese, diabetics who already have a significantly higher risk of the issue (though still low). I’m not a medical professional, but this doesn’t seem to be a concern that I would rationally want to spend a lot of time worrying about.

Diabetes mellitus (DM) is a common comorbidity in Fournier’s gangrene with a higher risk of mortality and longer hospital stays in these patients due to the microvasculature of many soft tissues and organs being affected

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8846449/

The main risk factors for Fournier’s gangrene are diabetes, obesity, immunosuppression (such as HIV), alcoholism, smoking, male sex, and the use of cytotoxic drugs [2]. Although many of the associated comorbid risk factors are common diseases, FG is rare. The published literature on its incidence in men and women is quite limited. Therefore, analysis from the US Inpatient Database of 593 civilian hospitals in 13 states in 2001 and 21 states in 2004 report that Fournier’s gangrene occurs in 1.6 of every 100,000 males per year, primarily between 50 and 79 years (3.3 of every 100,000).

The risk of Fournier’s gangrene in healthy people (i.e. you’re not an overweight, smoking diabetic) seems to be much less than 1 in 100,000. If it increases risk slightly while making 99,999 people live 15% longer, I think that is a trade-off most societies would take. Your own risk calculations may vary.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9141785/

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Yes, gangrene is usually a symptom of serious diabetes. If I were pre-diabetic or non-diabetic, I wouldn’t be worried about it. Although anything is possible.

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Thanks for presenting these data. Fourniers gangrene is not the only side effect of these medications as you know, just one of the most catastrophic when it does occur. I’m a bit biased because I have seen this occur in the hospital where I’m employed.

That said, I didn’t suggest that the OP stop the SGLT2 inhibitor because of this risk. I suggested it due to his self reported problems with waking up to void multiple times a night. Might be worth it to see if his sleep improves off of the drug no?

Just thinking out loud here but if the SGLT2 inhibitor pushes glucose into urine doesn’t that potentially feed any tumours which might be growing in the prostate?

I don’t think the prostate is directly exposed to urine normally, but maybe this could happen if you have a tear in the urethra or if one was urinating while upside down, causing some urine to travel up the vas deferens.

Perhaps your concern is relevant to bladder cancer, but I think the risk of bacterial infection is much more relevant as discussed above. Maybe it would be good to combine a UTI inhibitor like cranberry juice with SGLT2i’s, even if one doesn’t get full blown gangrene, it would be beneficial to limit bacterial growth that can cause inflammation/infection.

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