SNK
#883
the stuff you get from it is best sourced by natural, organic food. too expensive also.
Bicep
#884
If you really want to get proper nutrition, it requires doing what Lustgarten does and itâs a full time job. Nobody really has these answers. Nutrition is the wild wild west. So if there is a market for a complete feed (like we give to confinement animals) and they use it and sell it eventually it could be good. And we can spend our time and energy on other things. So I encourage this attempt and wish them well.
2 Likes
AnUser
#885
Not at all you can base your nutrition decisions on randomized controlled trials and the totality of evidence from epidemiological studies that control for many confounding factors.
Bicep
#886
Yeah, but you would need to do trials on humans at different ages with different levels of nutrients. All the nutrients. And the humans have different DNA, so at this point the totality of evidence amounts to around zero.
Feeding animals in confinement, like we do pigs, gives very useful information. They are in a closed room on a concrete or plastic slatted floor (so the poop can get away) and eating only what is in the feed. It took years to get this right, but I have to admit theyâre really efficient now. Not optimized for longevity, but really efficient.
From Chris Linnell on X
âIn this paper, researchers have found in male mice that SGLT2 inhibitors, used to treat diabetes, âreduced the senescence load in visceral adipose tissue and improved adipose tissue inflammation and metabolic dysfunctionâ.
Link in image
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Bicep
#888
That would explain some of the very nice pleiotropic effects wouldnât it?
Considering most senescent cells reside in adipose tissue, this is a very big deal for senescent cell load!
2 Likes
SGLT2 inhibition eliminates senescent cells and alleviates pathological aging
https://www.nature.com/articles/s43587-024-00642-y
5 Likes
adssx
#891
Unless I misunderstood, the paper does not prove that SGLT2 inhibition âeliminates senescent cells and alleviates pathological agingâ. It proves that canagliflozin does so. But it might be due to SGLT1 inhibition or to an off-target pathway. The only way to prove that itâs not SGLT1 inhibition would be to do the same study with empagliflozin (it could still be off-target, though).
5 Likes
adssx
#892
This paper might actually answer my question above: SGLT2i Alleviates Atherosclerosis by Inhibiting NHE1 Activation to Protect against Macrophage Senescence Induced by Angiotensin II 2024
(1) The formation of AS plaques in ApoE -/- mice showed a downward trend under DAPA. (2) After the intervention of Ang II, the cell activity of RAW264.7 decreased, and the expression of senescent cells and related genes increased. (3) Under the Ang II condition, the expression of SGLT2 and NHE1 increased, and SGLT2, NHE1, and senescence-related genes decreased with the addition of DAPA. (4) The expression of NHE1, senescent cells and related genes decreased in RAW264.7 cells after DAPA treatment with plasmid NHE1 intervention.
Dapagliflozin only has limited SGTL1 inhibition potency, so itâs most likely not SGLT1.
5 Likes
This also suggests a potential for additive/synergistic (or possibly just redundant) effect of angiotensin II inhibition (ARB or ACEi) in this process.
3 Likes
adssx
#894
Yes: Combining renin-angiotensin system blockade and sodium-glucose cotransporter-2 inhibition in experimental diabetes results in synergistic beneficial effects 2024
RAS blockade and SGLT2 inhibition display synergistic beneficial effects on BP, kidney injury and cardiac hypertrophy in a rat with hypertension and diabetes. The synergy does not involve upregulation of angiotensin-(1â7), but may relate to direct RAS-independent effects of empagliflozin in the heart and kidney.
5 Likes
I personally have a feeling that Telmisartan and Empagliflozin may have a lifespan extension potential similar to Rapamycin and Acarbose.
Iâll do both pairs. 
5 Likes
adssx
#896
Empagliflozin alleviates neuroinflammation by inhibiting astrocyte activation in the brain and regulating gut microbiota of high-fat diet mice 2024
EF alleviates neuroinflammation via improved gut microbiota profile and affects the Akt-mTOR pathway.
Sodium-Glucose Cotransporter 2 Inhibitor Improves Neurological Outcomes in Diabetic Patients With Acute Ischemic Stroke 2024
Our study showed that SGLT2i may be safely used without increasing END after AIS. Remarkably, acute phase SGLT2i use was significantly associated with better neurological outcomes at 3 months, while acute outcomes at discharge were not affected. Continuing SGLT2i use beyond discharge, rather than transient use during admission, was associated with a more favorable 3-month functional outcome.
In conclusion, our findings suggest that SGLT2i may be a priority for diabetic patients with AIS because of its potential benefits on neurological outcomes.
3 Likes
Neo
#897
Unusually favorable commentary by mainstream, top physician-scientist:
9 Likes
I know why it reduces mortality besides the senolytic effect. High glucose in serum = fat gain = plaque buildup in arteries of the brain, kidneys, and heart. When I get a Urinalysis, it is with great pleasure that when I read the report, the excertion of glucose from my body is off the charts.
4 Likes
adssx
#899
Impact of Sodium-Glucose Cotransporter-2 Inhibitor use on peak VO2 in advanced heart failure patients 2024
Our study is the first to compare before and after peak VO2 values of the OMT+SGLT2i group to the patientâs own baseline and we found no significant improvement.
2 Likes
AnUser
#900
No, thatâs not the way since other drugs that lower serum glucose does not have this effect.
1 Like
SGLT2 inhibitors are the only ones that actually removes the glucose from the body continously all day long in the urine. Get a urinalysis and you will see the numbers off the chart.
AnUser
#902
I know they reduce glucose via the urine, but you said it was because it reduced blood glucose.
