Please share any measures you think you can point to…
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Yes, with pleasure. For me, it is difficult to run in zone 2 at a meaningful speed. Even a minimal slope in “my” forest, where I always run, would catapult me into zone 3 or even higher. On the days when I take empagliflozin, my heart rate in cardio mode drops by 10-15 beats per minute, allowing me to run at a higher speed or overcome slopes without having to walk or leave zone 2 (which, in my case, ends around 130 bpm). And for those, who has difficulties running in zone 2 - knows, that is big change.
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@adssx - hmm, I read it as SGLT2i inhibiting cancer formation. If SGLT2 is overexpressed in cancer, inhibiting it seems like it should inhibit cancer rather than promote. And if SGLT2i promote T-cell infiltration of the tumor, then it’s promoting an immune response, and so increaing survival of the patient. That’s how I read it, but if course I could be wrong.
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Have you noticed a reduction in your resting heart rate on empagliflozin?
No, no noticeable changes. My resting HR is already rather low with 53 bpm, and no further improvement. It seems, that empagliflozin improves for me efficiency or cardio system.
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adssx
#961
Role of Glucagon in the Effects of Sodium-Glucose Co-transporter 2 Inhibition on Potassium and Magnesium Homeostasis 2024
We have reported that initiation of SGLT2 inhibitors can dramatically improve severe hypomagnesemia in patients with or without diabetes. As noted in a recent review, meta-analyses of randomized clinical trials have reinforced that SGLT2 inhibitors decrease the risk of hyperkalemia and correct hypomagnesemia.
Sodium/Glucose Cotransporter 2 Inhibitors and Magnesium Homeostasis: A Review 2024
The beneficial effect of SGLT2 inhibitors on magnesium balance in patients with diabetes with or without hypomagnesemia has been noted as a class effect in recent meta-analysis data from randomized clinical trials. Some reports have demonstrated their role in treating refractory hypomagnesemia in patients with or without diabetes.
Comparing clinical outcomes in patients with type 2 diabetes mellitus after ischaemic stroke: Sodium–glucose cotransporter 2 inhibitors users versus non-users. A propensity score matching National Cohort Study 2024
After propensity score matching, compared with the non-SGLT2i group (n = 2813), the SGLT2i group (n = 707) exhibited significantly lower recurrent IS rates (3.605% per year vs. 5.897% per year; hazard ratio: 0.55; 95% confidence interval: 0.34–0.88; p = 0.0131) and a significant reduction in all-cause mortality (5.396% per year vs. 7.489% per year; hazard ratio: 0.58; 95% confidence interval: 0.39–0.85; p = 0.0058). No significant differences were observed in the rates of acute myocardial infarction, cardiovascular death, heart failure hospitalization, or lower limb amputation.
Sodium-glucose co-transporter-2 inhibitors versus dipeptidyl peptidase-4 inhibitors on major liver outcomes in metabolic dysfunction-associated steatotic liver disease 2024
Among 44 651 patients, 22 100 initiated SGLT2is, and 22 551 began DPP4is. After weighting, the incidence rate of MLO in the SGLT2i group was 3.8 per 1000 person-years, and it was 3.9 per 1000 person-years in the DPP4i group, resulting in an adjusted hazard ratio (aHR) of 0.82 (95% CI, 0.60-1.10). SGLT2i initiation was not associated with cirrhosis (aHR: 0.77; 95% CI, 0.55-1.06) or hepatocellular carcinoma (aHR: 0.99; 95% CI, 0.47-1.83) separately. Subgroup and sensitivity analyses did not yield significant results.
Our study helps fill this knowledge gap by indicating that SGLT2is do not lower the risk of cirrhosis or HCC compared with DPP4is. This finding is in contrast to previous research, including a systematic review and meta-analysis of randomized controlled trials showing that dapagliflozin improves liver studies, such as alanine aminotransferase (ALT) and aspartate aminotransferase levels,31 and the E-LIFT trial, which found that empagliflozin reduces liver fat and improves ALT levels in T2D and MASLD patients.
Disappointing paper on liver function. However, all the HR, even though not statistically significant, are on the side of SGLT2i benefits. We’ll have to wait for the ongoing trials of SGLT2i in NAFLD…
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adssx
#962
Impact of Sodium-glucose Cotransporter 2 Inhibitor on Recurrence and Cardiovascular Outcomes after Catheter Ablation for Atrial Fibrillation in Patients with Heart Failure 2024
SGLT2i was associated with a lower risk of AF recurrence (adjusted HR = 0.56, 95% CI: 0.43-0.74, P<0.001). The composite risk of cardiovascular death, thrombotic events, or cardiovascular hospitalization was significantly lower in the SGLT2i group compared with those without SGLT2i (adjusted HR = 0.58, 95%CI: 0.41-0.80, p = 0.001). Although there was a trend toward benefits, the differences in all-cause mortality, cardiovascular death, or thrombotic events were insignificant between the 2 groups.
SGLT-2 inhibitors are beneficial in reducing the risk of thyroid cancer: findings from a Mendelian randomization study 2024
In European populations, SGLT2 inhibitors were significantly negatively associated with TC (OR 0.051, 95% CI 0.006–0.465, P = 0.0082) as well as PTC (OR 0.034, 95% CI 0.003–0.411, P = 0.0079), while no correlation was found with FTC. These findings remained consistent even after applying the Bonferroni correction.
That OR!!!
Efficacy of Sodium-Glucose Cotransporter-2 Inhibitors in Patients With Acute Myocardial Infarction: A Meta-Analysis of Randomised Controlled Trials 2024
Five RCTs reporting data for 11,211 patients were included in our study. The mean follow-up duration was 43.8 weeks. Our pooled analysis showed that SGLT2 inhibitors significantly reduced the risk of hospitalisations for heart failure (HHF) (RR = 0.76, 95% CI: 0.61–0.88, p = 0.001) in patients with MI. However, the risk of all-cause mortality (RR = 1.05, 95% CI: 0.78–1.41, p = 0.76), CV mortality (RR = 1.04, 95% CI = 0.84–1.29, p = 0.73) and all-cause hospitalisations (RR = 1.06, 95% CI: 0.96–1.17, p = 0.25) remained comparable across the two groups.
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on a potentially negative note, I think one of the meds I’ve been taking out of jardiance/rapa/telmisartan/simvastatin/ezetimibe/acarbose may have been contributing to some noticeable muscle loss for me. I’m suspecting the jardiance?
https://www.nature.com/articles/s41598-022-21486-9
I’ve read statins could potentially be at play as well. is this something to watch for?
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What has been your typical exercise regimen during the time you’ve been taking the medications?
Body by science, which is one strength training day a week. The program believes one set to failure can maximize growth.
I’ve been on it for the past 4 years though, no change. And there has been no change in diet. I’m getting older of course, about to be 46. I guess growth can slow with age?
One difference is I’ve been taking glycine on/off which should actually help with growth I believe
The loss has been IMO slow but accumulative. I wasn’t sure at first, but its gotten to the point where its a bit noticeable
If you’re worried about muscle loss and only strength training one day a week, most training literature would suggest that optimal strength training frequency would be at least 2-3 days per week.
That would be a decent place to start if you’re concerned about keeping a healthy amount of muscle as you get older.
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Davin8r
#967
Latest research says 10-20 sets per muscle per week ( higher volume causes even more gains but diminished returns and harder to recover from), only going to failure in the final set (otherwise “close to failure” for the other sets). Rep ranges from 5-30, even higher is ok but much more painful. Compound movements like the bench press count as 1 set for chest and 1/2 set for triceps, for instance. I follow Wolf Coaching on YouTube. He’s an actual PhD researcher who is actively publishing studies.
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mccoy
#968
Sunshine4 refers to a training regime supported by the likes of Mike Mentzer and Dorian Yates, presently by a few trainers, where muscle hypertrophy is stimulated by providing an intermittent signal of maximum intensity, but low frequency, to allow for recovery.
Dorian Yates won 6 Mr Olympia with this method, whose drawback in my opinion is that it may overstress tendons, ligaments and joints and not be ideal at older ages. Injuries can be a real threat.
However, it has been shown to trigger hypertrophy, if executed correctly.
adssx
#969
The effect of SGLT2 inhibition on prostate cancer: Mendelian randomization and observational analysis using electronic healthcare and cohort data
Using Mendelian randomization, we found that genetically proxied SGLT2 inhibition reduced the risk of overall (odds ratio = 0.56, 95% confidence interval [CI] = 0.38 to 0.82; 79,148 prostate cancer cases and 61,106 controls), advanced, and early-onset prostate cancer. Using electronic healthcare data (nSGLT2i = 24,155; nDPP4i = 24,155), we found that the use of SGLT2 inhibitors was associated with a 23% reduced risk of prostate cancer (hazard ratio = 0.77, 95% CI = 0.61 to 0.99) in men with diabetes.
Powerful finding combining Mendelian randomization and longitudinal data: quite convincing. I wonder if we have animal models + potential mechanistic pathway as well.
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I may have misunderstood the original poster, but Dorian Yates worked out 4 days per week, not just one. Only 1 day per week of strength training will very likely not be enough to maintain adequate muscle as we age.
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mccoy
#971
sluggerT80, yes yesterday I listened to Dorian Yates’ podcast interviewing Peter Attia, he says he trained about that amount but one hour per session. Compared to other Olympians, that’s a tiny amount.
I also searched Hi-intensity workouts when I started training again 7 years ago.
What follows is OT but maybe clarifies some concepts.
The rationale is to train at extremely high intensity, few sets and then rest to recover. Good for busy people. I read Mike Mentzer, I read other trainers, but I gave up searching soon after I realized that hi intensity means just that, lifting the highest loads to yield the highest growth signal, then resting no matter how long it takes.
This is not what the eminent authors in this field, like Brad Schoenfeld, suggest. Also, I think it’s not at all suited to more aged people. Dorian Yates underwent several injuries.
One of the bodybuilders who aged best is maybe Lee Haney, who would lift relatively moderate loads.
Presently, I follow a highly individualized scheme, lifting many sets to failure, but only the loads which do not cause any pain, ache or inflammations to my muscles and tendons.
I wish I could lift heavy weights for hours and recover expeditiously but at 64, having undergone 25 years of inactivity and an existing hernia I understood I must cool down substantially.
Davin8r
#972
I wouldn’t follow the personal training advice of professional bodybuilders on anabolic steroids unless perhaps you’re also taking anabolic steroids. I’d follow the research that is actually published in peer-reviewed scientific journals on subjects who aren’t taking steroids. See my post above for summary of the very latest.
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mccoy
#973
I agree and my best suggestion for a reading is Brad Schoenfeld’s book. I don’t know Wolf coaching but he says just about the same things written in the book (I have the 1st edition).
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Davin8r
#974
Yep Schoenfeld is pretty much THE guru of hypertrophy training and I have both editions of his book. Wolf knows him and has interviewed him, but Wolf also is carrying the torch and publishing new stuff.
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I intend to get on empagliflozin, as my blood glucose numbers are steadily getting worse despite my best diet/lifestyle efforts. My numbers right now are prediabetic, moving toward diabetic, FBG in the 110-115 range in the morning, A1c 5.9; this has been going on for 5 years or so, every year getting worse. At one point I was on metformin 500mg/day, which did absolutely nothing. I stopped the metformin, because I don’t like what the alleged effect is on exercise. I’m a 66 y/o caucasian male, and I intend to get on acarbose first, which I anticipate will do very little for my glucose control, and once I establish that after another A1c test 90 days later, I will get on 10mg/day empagliflozin. I anticipate that will happen next year soon after I turn 67.
In case empagliflozin is well tolerated by me, and has a favorable effect on my FSB and/or A1c, I was wondering how people use it - in particular, is there any indication as to how LONG TERM use works, and do people take breaks from use, or what. FWIW, I don’t have any medical conditions, only my lipid, BG, BP numbers are all moving in the wrong direction, so I want to nip it in the bud. TYIA!
