Hi All, Much tnx to such fine data/discussion as always. Bought Dapa from India (same person we all use for cheap so not married to my stash).
Empa vs Cana vs Dapa vs? I did a google some time ago and guessed Dapa had fewer side effects may have been wrong.
Admin here moved to Empa, probably for good reasons (hopefully other then possible cost?).
I have alternated taking 5mg Dap (10mg split) both / alternating with 250mg metformin at night. Night to attampt to avoid the possible fatigue and mainly to benefit from thymus gland rejuvination.
As tipped by rejuvination health coach Alex Kikel (search on youtube).
Rethinking my fatigue test maybe I need to test taking metformin at noon after feeling perky in the AM to see if I roll over. Then same experiment with dapa at noon. I was taking dapa early AM in a blender (canāt swallow pills).
I eat very low carb so I may be teasing my body with night / day hypoglycemic events un-wittingly. I need to find my lost CGM stash.
Mainly any terse summry of this wise groups preference for which SGLT2 without regard to cost or difficulty getting, assuming some lower dose since Iām low carb, zero fruit, only for anti aging.
Empagliflozin Improves Insulin Sensitivity of the Hypothalamus in Humans With Prediabetes: A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Trial
āOur results corroborate insulin resistance of the hypothalamus in humans with prediabetes. Treatment with empagliflozin for 8 weeks was able to restore hypothalamic insulin sensitivity, a favorable response that could contribute to the beneficial effects of SGLT2 inhibitors. Our findings position SGLT2 inhibition as the first pharmacological approach to reverse brain insulin resistance, with potential benefits for adiposity and whole-body metabolism.ā
SGLT2 inhibitor use was associated with a 20 % lower risk of all-cause dementia compared to DPP-4 inhibitors.
Strongest effects observed in patients >80 years and male patients.
SGLT2i showed a significant reduction in unspecified dementia but not in Alzheimerās or vascular dementia.
Yes, almost certainly the reason. Not a problem unless high (maybe over 52 or 54?) although cutoff isnāt clear, and maybe even then not much of a problem unless there are other risk factors for arterial/venous thrombosis. And it can certainly be a positive if hematocrit is too low.
Iām at 48.2 - according to LabCorp, itās still within their reference interval 37.5 - 51, so I figure as long as I keep adequately hydrated I should be fine.
You are golden at 48. My most recent was 53, so I stopped empagliflozin for the time being. If normalized, Iāll start back on a 1/2 dose of dapagliflozin, since unlike empa its Hct-raising property is dose-dependent.
A perk to stopping empagliflozin is only having to get up once at night to pee instead of 2 or 3(!). Iāll definitely have to weigh the sleep impairment against the potential health benefits in deciding whether to continue using an SGLT2i long-term.
Do you think it could be safe to take mirabegron to reduce awakenings and also burn fat at the same time? Or is it harmful to keep the glucose-enriched urine in the bladder?
I actually tried Mirabegron and was really disappointed when it didnāt work for me, for whatever reason.
I have desmopressin on deck to try, but it can increase risk of thrombosis so Iāve put it off for the time being, especially with my hematocrit borderline-high.
Thx for sharing! I never knew Alex was so young! Iām jealous :). And I forgot that I used to have the Wolfram app, but somehow along the way, I forgot about it. Nice to see the man behind it.
Your question prompted me to do some digging. I actually tried Vibegron (Gemtesa 75mg), which is a newer/better cousin of mirabegron, but critically, I only tried it for 30 days because I assumed at the time that the benefits would be nearly immediate. In fact, it takes a full 12 weeks for max benefit based on the clinical trials, so I feel stupid for my assumption but also now hopeful that it will work when I try it again. Iām not worried about UTIs from taking it with an SGLT2i because Iām fully immunocompetent and Iāve never had issues with UTIs even when I had severe prostate enlargement, but if I had a different history then I can see how it might be an issue.
Youāre probably aware of the off label use also. Open Evidence says mirabegron activates brown adipose tissue and increases resting energy exposure, but it says vibegron has not been shown to do the same. Maybe it just hasnāt been studied, though.
The administration of 200 mg per day of oral mirabegron for 12 weeks to 12 healthy men was associated with higher BAT activity (measured via 18F-fluorodeoxyglucose positron emission tomography combined with computed tomography) and the elevation of the resting metabolic rate by 203 Ā± 40 kcal/day, compared to individuals receiving the placebo.
But nothing is free:
It was reported that high doses of mirabegron (especially 200 mg per day), much higher than those approved by the FDA for bladder overactivity (50 mg per day), may be associated with cardiovascular side effects such as headaches, tachycardia, and elevated blood pressure (mostly only systolic blood pressure)
Risking cardio health with high dose beta-3 agonists would seem unwise since there are so many other options for fat loss these days, but I get it that some who have more issues than I do with losing body fat might need a multi-pronged approach. Personally, Iād be happy with being able to take an SGLT2i and not have to get up to pee at night (while also keeping hematocrit under control).
No, itās too dangerous, and why I put the block quote there about the risk. The BP increase is substantial. But at therapeutic doses, it still beiges white adipose tissue! And thereās speculation that there may still be a small, cumulative metabolic effect over time.
