Creatine Supports AMPK Activation and Increases Longevity in Lab Animals
by Nils Osmar. October 3, 2022. Medical Disclaimer
According to some recent studies, creatine may not only build muscle, it increases AMPK and is associated with a significant extension of lifespan.
- Study 1: Creatine activates AMPK (the longevity pathway)
- AMPK is an enzymatic pathway associated with longevity. In animal studies, activating AMPK correlates with longer lifespans
- See study: Creatine supplementation increases glucose oxidation and AMPK phosphorylation and reduces lactate production in L6 rat skeletal muscle cells
From the study:
We conclude that 48 h of creatine supplementation does not alter insulin-stimulated glucose uptake and glucose metabolism; however, it activates AMPK, shifts basal glucose metabolism towards oxidation and reduces lactate production in L6 rat skeletal muscle cells
Another study
According to this study, mice given creatine live 9 percent longer than control animals
Recently, creatine has been found to significantly lower the accumulation of a recognized marker of aging called lipofuscin in the brains of aging mice. As a result, creatine-fed mice lived an average of 9% longer than control animals— that’s equivalent to more than seven years for an average human!
See study: Creatine Reduces Markers Of Aging – Life Extension
My thoughts – and what I’m doing
It makes sense to me that creatine would be associated with life extension, since AMPK has long been recognized by anti-aging researchers as the longevity pathway. (Longevity is associated in many different species with activating AMPK and dampening the activation of mTOR, a pathway associated with growth.)
My approach to life extension is to alternate between periods of activating AMPK and activating mTOR. (Both are needed, but studies suggest that AMPK should be activated most of the time.) We don’t want to permanently switch off mTOR, as it’s essential to both maintaining muscle mass, and to immunity. (Our immune systems atrophy and we’re more vulnerable to sarcopenia and dementia if we don’t have enough mTOR activation. But it’s clear that there are advantages to having if off periodically, for a given period of time.
Most people wake up in the morning with AMPK activated (because they’ve been fasting since the previous night’s dinner.) Skipping breakfast can then prolong the activation of AMPK. So can taking AMPK-activating supplements such as creatine, berberine, glucosamine and/or milk thistle.
For the past year or two, I’ve been taking my NMN and SIRT6 activator in the mornings; then workibg out; then taking creatine after my workouts.
I’m currently trying a variation on this, which is to take my NMN and SIRT6 activator around noon; then take creatine a half hour later; then work out. I take these supplements with a small scoop of a green powder with almost no protein or carbs, to enhance absorption without and danger of stopping my fast, stopping AMPK activation or stopping autophagy.
I then work out for about an hour, after which I have my first meal meal with protein around 2 or 3 pm. At this time, I stop trying to activate AMPK and eat a meal high in protein and leucine to switch on mTOR, the growth pathway. (I take my hGH boosters and testosterone boosters along with this meal.) I eat dinner around 7 or 8 pm, a five hour eating window.
The results
- The result (so far) is that I feel better energy than when I was taking my NAD boosters early in the morning, then working out around 8 or 9 a.m, then taking creatine after my workouts.
- I’ve been gaining a bit of unwanted fat around my middle for the past couple of months; I’m hopeful that making this change will support fat loss. It seems likely that it will, if only because my eating window is so much shorter.
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Other resources
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