On henagliflozin and telomeres, @Kelman mentioned there: “Why would placebo group have a 65% increase in telomere, that is huge? and how was it measured?”
Wdyt @Cole?
This is because both groups of participants received lifestyle interventions, including diet control, regular exercise, and overall healthy habits. But even so, the telomere length in the henagliflozin group was still significantly longer than in the control group. I think that really speaks volumes. For us biohackers who already stick to a healthy lifestyle, this makes it an absolutely top-tier drug. Of course, empagliflozin is also an excellent anti-aging drug, with practically flawless performance in its cardiovascular outcome trials.
For telomere measurement, they used qPCR. Its reliability is relatively mediocre—while it isn’t state-of-the-art, it remains the most widely used method. Currently, the most advanced technique is arguably TeSLA.
I accept this paper, warts and all.
I’m sorry I didn’t read your whole response, but the telomere growth rate in the control group was actually 6.67%. Anyway, I support people taking whatever medications they want to take.
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Indeed @Kelman: the paper says 65.57% of placebo participants had any increase in measured leukocyte telomere length but the placebo arm’s increase was around +6–7%, not +65%. The henagliflozin arm was roughly +15%, with an incremental effect over placebo of about +0.06 T/S units.
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Longitudinal changes in leukocyte telomere length and mortality in elderly Swedish men
TL attrition did not predict all-cause or cancer mortality, but we found a 60% decreased risk for cardiovascular mortality in those who shortened their telomeres.
So is telomere lengthening the right metric?
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