I too had wildly inaccurate readings, constant low sugar alarms. Finger prick was always much higher on Abbott monitors and went through three of them, three out the last.
To Abbottās defense (but is it really to their defense?) and if I reckon correctly, you used an old model (that they re marketed as new and OTCā¦). Newest model are quite accurate.
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I did try Abbot once. (I think it was Libre 2) It didnāt seem inaccurate, but having to download the results every 8 hours to avoid losing data was a real nuisance. I have stuck to DexCom since.
Has anybody tried dexcom stelo? $100/ one month, this looks pretty good.
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!CAUTION!: Chinese paper.
This is in T2DM people. Empagliflozin might be mildly protective and canagliflozin might be problematic.
Relationship Between SGLT-2i and Ocular Diseases in Patients With Type 2 Diabetes Mellitus: A Meta-Analysis of Randomized Controlled Trials
āCompared with controls, overall SGLT-2i use in T2DM patients was not associated with incidences of cataract, glaucoma, retinal disease and vitreous disease. Ertugliflozin (RR=0.47, P=0.01) reduced the risk for retinal disease, while empagliflozin (RR=0.44, P=0.05) reduced the risk for diabetic retinopathy (DR) compared with controls. SGLT-2i (RR=0.50, P=0.02), perhaps empagliflozin (RR=0.47, P=0.06), reduced the risk of retinal disease compared with active hypoglycemic agents. Canagliflozin (RR=4.50, P=0.03) increased the risk for vitreous disease compared with placebo.ā
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More recent papers in better journals by better research teams (all cite the 2022 Chinese one):
Results: Our final analysis included 20,966 T2DM patients prescribed SGLT2 inhibitors and 20,966 prescribed DPP-4 inhibitors. Compared to the DPP-4 inhibitor group, the SGLT2 inhibitor group was associated with significantly lower risks of AMD (hazard ratio [HR], 0.71; 95% confidence interval [CI], 0.58ā0.85) and dry AMD (HR, 0.61; 95% CI, 0.46ā0.80) but not wet AMD (HR, 0.74; 95% CI, 0.48ā1.16). SGLT2 inhibitors compared with DPP-4 inhibitors were linked to a reduced risk of AMD in the White population, patients prescribed empagliflozin or dapagliflozin, and individuals with glycated hemoglobin < 8.5%, estimated glomerular filtration rate ā„ 60 mL/min/1.73 m2, hypertension, or dyslipidemia, regardless of body mass index level.
A significantly reduced risk of AMD is observed in patients prescribed empagliflozin and dapagliflozin rather than canagliflozin. Given that empagliflozin and dapagliflozin have a higher relative affinity for SGLT2 over SGLT1 compared to canagliflozin, our findings suggest that SGLT1 and SGLT2 may be expressed differently in the retina.
Harvard + UPenn: Sodium-Glucose Cotransporter 2 Inhibitors for the Primary Prevention of Glaucoma in Patients With Type 2 Diabetes: A Target Trial Emulation 2024
Patients on SGLT2i, compared with those on DPP4i, had a lower risk of glaucoma (hazard ratio [HR] 0.815, 95% confidence interval [CI] 0.794, 0.837), including open-angle glaucoma (HR 0.755, 95% CI 0.729, 0.781) and primary angle-closure glaucoma (HR 0.702, 95% CI 0.636, 0.781). Among all SGLT2i, ertugliflozin (HR 0.668, 95% CI 0.512, 0.871) was associated with the lowest risk of glaucoma, followed by empagliflozin (HR 0.727, 95% CI 0.696, 0.759), dapagliflozin (HR 0.814, 95% CI 0.774, 0.855), and canagliflozin (HR 0.893, 95% CI 0.862, 0.926). The protective effect of SGLT2i on glaucoma was validated when compared with GLP1RA (HR 0.932, 95% CI 0.906, 0.959).
Empagliflozin and the Risk of Retinopathy in Patients With Type 2 Diabetes 2024
Compared with initiation of a DPP4i, empagliflozin initiation was not associated with incident NPDR, although it may be associated with a lower risk of DR progression.
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Sadly Iāve decided to drop empagliflozin. Recently started on TRT and just wasnāt comfortable with my HCT creeping up into the 50ās. Has anyone managed to use both long term while keeping their HCT in check?
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@austin242 Iād encourage you to watch this video from a doctor who sees this all the time in his practice in testosterone users before making what I believe is a mistake.
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Introduction to TRT Concerns
- The video begins with an introduction to the topic of optimizing menās health through testosterone replacement therapy (TRT) amidst the challenges of the U.S. healthcare system.
- The speaker shares insights gained from discussions on popular TRT forums, highlighting three recurring issues that men frequently discuss.
Common Issues in TRT Forums
- The first major concern involves men expressing anxiety over their estrogen levels and the dosage of aromatase inhibitors prescribed by their doctors.
- The second concern revolves around inquiries about lowering sex hormone-binding globulin (SHBG), with many men discussing various methods suggested by clinics, although the speaker notes that lowering SHBG may not be necessary.
- The third issue is related to hematocrit levels, with numerous questions about blood donation frequency, what constitutes a dangerous hematocrit level, and concerns about clotting and thrombosis associated with TRT.
Hematocrit Levels and Misconceptions
- The speaker emphasizes that misconceptions about hematocrit levels and their relation to TRT persist despite the availability of accurate information from qualified professionals.
- Many forum users appear to rely on unverified advice, leading to confusion and anxiety about their health.
- The speaker stresses the importance of consulting medical professionals rather than seeking advice from social media forums, which can often provide misleading information.
Clotting Risks and Erythrocytosis
- The speaker discusses erythrocytosis, defined as an increase in red blood cell mass, and its potential connection to TRT, particularly with intramuscular testosterone injections.
- It is noted that a hematocrit level above 52 percent is often viewed as abnormal, while some clinics require blood donation once hematocrit reaches 50 percent, a practice the speaker considers unsupported by medical literature.
- The speaker refers to guidelines from the Endocrine Society regarding hematocrit thresholds and the management of TRT, highlighting the need for more nuanced understanding in clinical practice.
The Psychological Impact of Misunderstood Risks
- The psychological impact of perceived risks related to hematocrit and clotting is discussed, as many men worry excessively about their health based on inaccurate information.
- The speaker urges viewers to be proactive in seeking accurate medical advice and to communicate openly with their healthcare providers regarding any concerns they may have.
Understanding Clotting Risks
- The speaker outlines classic risk factors for thrombosis, including major surgery, previous clots, cancer, obesity, and certain medications like contraceptives.
- He emphasizes that while testosterone therapy is often blamed for clotting events, many individuals have underlying hereditary conditions that contribute to their risk.
- The speaker also mentions that testosterone therapy has not been consistently shown to increase the risk of venous thromboembolism (VTE) in otherwise healthy men.
Research on Testosterone and Clotting
- The speaker references multiple studies indicating that testosterone therapy does not significantly increase the risk of thrombotic events compared to the general population.
- He highlights a large meta-analysis that concluded TRT is not associated with an increased risk of venous thromboembolism, reinforcing the need for evidence-based practice.
- The speaker also mentions a study specifically examining men with hypogonadism, which found no significant association between testosterone therapy and thrombotic events.
Conclusion and Recommendations
- In conclusion, the speaker urges men to avoid seeking medical advice from unqualified sources on social media and to prioritize consultations with their healthcare providers.
- He encourages viewers to advocate for their health by asking their doctors questions and seeking clarification on any uncertainties regarding their treatment.
- The video ends with a call to action for viewers to share their experiences with hematocrit management in TRT and to stay informed about their health.
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Thanks. Some useful datapoints here. But I believe there was also a study posted just a few days ago in this thread indicating that TRT users who developed polycythemia (Hct ā„52% within the first year) had a 35% higher risk of MACE/VTE compared to TRT users without polycythemia
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Make sure you drank enough water or were properly hydrated your last blood draw. Thatās usually one of the most common reasons for a higher hematocrit (although I disagree with the idea that 50 is high). Simply drinking enough water or getting it checked later in the day can have a dramatic effect.
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True. It was 51 which isnāt terrible but Iām also only 5 weeks into TRT so I expect it may continue to rise a bit
Other things you can try for lowering hematocrit, instead of stopping the empagliflozin:
- increasing aerobic exercise
- ACE inhibitor or ARB
- daily microdose TRT instead of weekly/biweekly
- making sure you donāt have sleep apnea (and getting treated if you do)
- changing to low dose dapagliflozin, since dapa-induced Hct elevation is dose-dependent whereas empagliflozin is not (same degree of elevation at 10mg vs 25mg dose)
Once my Hct comes down to a comfortable range, Iām going to try low-dose dapagliflozin and monitor closely.
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Very helpful thanks. Where is your HCT now and what do you consider a comfortable range?
Itās 52 now, so Iād like to get it down to maybe 50 or lower, then Iāll add the dapa and see. Iād be happy with less than 52 for long-term maintenance, but I have cardiac risk factors so I may need to be more cautious than the average person. I just stopped empa a week ago, and it could take up to 3 months for the Hct elevation to fully reverse (but Iāll be getting it checked much more frequently since Iām doing all of the above as well).
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Mine is 50 on 25 of empagliflozin, no TRT.
Youāre safe. The increased Hct from SGLT2i alone does not result in increased risk of DVT, as explained by OpenEvidence:
"Increased hematopoiesis caused by empagliflozin does not lead to a higher risk of deep vein thrombosis (DVT) because the mechanism is driven by enhanced erythropoiesis rather than hemoconcentration, and clinical data show no increase in thromboembolic events. Empagliflozin stimulates erythropoietin production, leading to a gradual rise in red blood cell mass and hematocrit over several months, rather than a rapid plasma volume contraction that could acutely increase blood viscosity and thrombosis risk.[1-4] This distinction is critical: hemoconcentration from diuresis can transiently increase thrombosis risk, but the sustained hematocrit increase from empagliflozin reflects improved erythropoiesis and iron mobilization, not dehydration or hypercoagulability.
Large randomized controlled trials and pooled safety analyses consistently demonstrate that the incidence of DVT and other venous thromboembolic events is similar between empagliflozin and placebo groups, even as hematocrit rises.[1][5-7] Table 2 from the EMPA-REG OUTCOME trial directly shows that thromboembolic event rates do not differ between groups, supporting the safety of empagliflozin with respect to DVT risk."
So then my question would be, does this mean we can ignore the contribution of increased Hct from an SGLT2i while on TRT? @DrFraser , do you have any experience in this area?
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Empagliflozin Protects Against Oxidative Stress in the Diabetic Brain by Inducing H2S Formation 2025
Background: Hydrogen sulfide (H2S) is an endogenously produced gaseous neurotransmitter. H2S donors exhibited neuroprotection in oxidative-stress-related disorders in preclinical studies, but odor and short half-lives have limited their clinical use. However, endogenous H2S stimulators with antioxidant properties have advantages over H2S donors regarding safety and patient compliance. Empagliflozin (EMPA), a sodiumāglucose cotransporter-2 (SGLT2) inhibitor widely used in the treatment of diabetes mellitus (DM), exerted similar neuroprotective and antioxidant effects as H2S and shares common mechanisms. This study aimed to investigate the role of H2S in the antioxidant effects of EMPA in the brain.
Methods: The effects of EMPA on H2S production and reactive oxygen species (ROS) formation were assessed ex vivo in mouse brain under normal conditions and pyrogallol-induced oxidative stress. Moreover, rats were divided into the following four groups: nondiabetic, EMPA-treated nondiabetic, streptozotocin (STZ)-induced diabetic, and EMPA-treated, STZ-induced diabetic. Endogenous H2S and ROS levels in the brain were measured using methylene blue and chemiluminescence assays, respectively.
Results: Ex vivo EMPA treatment significantly increased endogenous H2S formation in both healthy and pyrogallol-induced oxidative stress, as well as reduced ROS formation in mouse brain; these effects were significantly reversed by the H2S synthesis inhibitor aminooxyacetic acid (AOAA). Oral EMPA administration significantly elevated brain H2S levels in both nondiabetic and diabetic rats and reduced ROS formation. These effects were inhibited by AOAA.
Conclusions: Our study revealed a novel mechanism by which EMPA can reduce oxidative stress in neurodegenerative disorders by triggering H2S synthesis in the brain.
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Iām not sure we have the exact data on that - but a Hct of >54% is a reason to hold doses of testosterone, generally, until it is below 50%. Itās not just venous side risk (DVT/PE) that is a worry it is the arterial side also with stroke and myocardial infarction with the higher Hct.
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How did we specifically land on >54% hematocrit (w/ no other risk factors) as the cutoff number that determines that the risk of a cardiovascular issue is greater than the risk of a cardiovascular issue from being hypogonadal?