Researchers Discover How Caffeine Could Slow Cellular Aging (phys.org) 26
alternative_right shares a report from Phys.Org: In new research published by scientists studying fission yeastâ"a single-celled organism surprisingly similar to human cellsâ"researchers found that caffeine affects aging by tapping into an ancient cellular energy system. A few years ago, the same research team found that caffeine helps cells live longer by acting on a growth regulator called TOR (target of rapamycin). TOR is a biological switch that tells cells when to grow, based on how much food and energy is available. This switch has been controlling energy and stress responses in living things for over 500 million years. But in their latest study, the scientists made a surprising discovery: Caffeine doesn't act on this growth switch directly. Instead, it works by activating another important system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.
"When your cells are low on energy, AMPK kicks in to help them cope," explains Dr. Charalampos (Babis) Rallis, Reader in Genetics, Genomics and Fundamental Cell Biology at Queen Mary University of London, the study's senior author. "And our results show that caffeine helps flip that switch." Interestingly, AMPK is also the target of metformin, a common diabetes drug that's being studied for its potential to extend human lifespan together with rapamycin. Using their yeast model, the researchers showed that caffeine's effect on AMPK influences how cells grow, repair their DNA, and respond to stress -- all of which are tied to aging and disease. The study has been published in the journal Microbial Cell.
"When your cells are low on energy, AMPK kicks in to help them cope," explains Dr. Charalampos (Babis) Rallis, Reader in Genetics, Genomics and Fundamental Cell Biology at Queen Mary University of London, the study's senior author. "And our results show that caffeine helps flip that switch." Interestingly, AMPK is also the target of metformin, a common diabetes drug that's being studied for its potential to extend human lifespan together with rapamycin. Using their yeast model, the researchers showed that caffeine's effect on AMPK influences how cells grow, repair their DNA, and respond to stress -- all of which are tied to aging and disease. The study has been published in the journal Microbial Cell.
Hot damn. (Score:5, Funny)
The years of caffeine abuse might just might level out the alcohol years. Look at me living a balanced life!
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Balance is important [wikipedia.org] ;-)
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It's rum and coke from here on out.
For those hard nights, 151 and Jolt.
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Providing my heart doesn't explode from the speed at which it beats after drinking 10 cups a day I should be able to live forever!
Well then (Score:1)
Shit! (Score:3)
AMPK (Score:3, Informative)
Its probably hard to overstate AMPK's contribution towards health. It appears to regulate a great number of other systems. There's another isoform of AMPK that appears to activate on starvation, tying it in with intermittent fasting. mTOR is often dysfuctional in cancer, and with AMPK deactivating mTOR, its a logical target. Adelfo at Suppversity has a great series on AMPK and mTOR. Recommend reading these links as a summary couldn't capture all the info https://suppversity.blogspot.c... [blogspot.com] https://suppversity.blogspot.c... [blogspot.com] https://suppversity.blogspot.c... [blogspot.com]
In the last installments of this series we have begun to dig deeper into the signaling mechanisms that are / could be involved in the beneficial effects intermittent fasting is hailed for in the (unreal) world of the Internet blogosphere. We have identified AMPK and mTOR as the two players in the constructive and de-/re-constructive orchestrate of mammalian organisms and we have learned that their relationship - despite all its antagonistic aspects - is, after all, a complementary one. This means that, as you can observe it time and again in nature, health, vitality, yes even sustainable changes in body composition require balance!
The delicate balance between mTOR and AMPK, this was another result of our considerations, is oftentimes broken in these days of nutritional abundance, where the rebuild and repair mechanisms of AMPK hardly get a chance to control the growth processes a constantly elevated mTOR pathway is triggering. The forced feeding-breaks on an intermittent fasting regime break this rampantly anabolic cycle. They let AMPK come into it's own and allow for
.....broken DNA strands to be fixed, before their (re-)use results in cancerous growth (Habib. 2010),
In the previous episode, we have also identified energy availability or, to be precise, the ratio of the high energy ATP (adenosine triphosphate) to the lower energy ADP (adenosine diphosphate; -7.3kcal/mol) and AMP (adenosine monophosphate; -10.9kcal), as a crucial determinant of AMPK activation. In one of the most recent reviews on the topic (Carlin. 2011), David Carlin and colleagues from the Imperial College in London state that
[...] the finding that ADP, as well as AMP, protects AMPK against dephosphorylation influences the way we look at the physiological regulation of AMPK. To the best of our current understanding, the concentration of ADP in mammalian cells is much higher (10- to 100-fold) than that of free AMP, and so it is likely to be the main regulator of AMPK activity under normal energy-stress conditions. The extent of the tighter binding of ADP to AMPK, relative to MgATP, essentially offsets the higher physiological concentration of MgATP. An interesting possibility is that under most conditio
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The key sensor of energy status in mammalian cells, AMP-activated protein kinase (AMPK), can also be activated by the AMP analog aminoimidazolecarboxamide nucleoside monophosphate (ZMP) generated directly from aminoimidazolecarboxamide ribonucleoside (AICAR) or from inhibition of purine synthesis by the antifolate pemetrexed (PTX), a drug used extensively in the treatment of lung cancers. Despite this common mechanism, signaling downstream of AMPK activated by PTX or AICAR differed. AICAR-activated AMPK inhibited mTORC1 both directly by phosphorylation of the mTORC1 subunit Raptor and indirectly by phosphorylation of the regulator TSC2. In contrast, PTX-activated AMPK inhibited mTORC1 solely through Raptor phosphorylation. This dichotomy was due to p53 function. Transcription of p53 target genes, including TSC2, was activated by AICAR but not by PTX. Although both PTX and AICAR stabilized p53, only AICAR activated Chk2 phosphorylation, stimulating p53-dependent transcription. However, Raptor phosphorylation by AMPK was independent of p53 and was sufficient, after PTX treatment, to inhibit mTORC1. We concluded that PTX effects on mTORC1 were independent of TSC2 and p53 and that the activation of a p53 transcriptional response by AICAR was due to an activation of Chk2 that was not elicited by PTX. https://pmc.ncbi.nlm.nih.gov/a... [nih.gov]
P53 activation is probably usually good, but there may be times that activation without p53 might be better, in say gain-of-function p53 cancers (where p53 doesn't do what its supposed to, but something else). And probably with 25-35 trillion cells, a number of our cells may be cancerous at this moment and our
When unstoppable bias, meets undeniable.. (Score:3)
Given the sheer amount of humans that are addicted to caffeine, are we sure we are still capable as a race to study this fairly, without obvious bias?
Before you answer, consider that the most affluent of caffeine junkies waits until a civit shits that coffee bean out of it’s ass first before they happily roast that recycled turd into a nice cuppa joe and drink it. I mean, damn. Even the “dirty” hippie is gagging. We think it takes bad leaders and corrupt politics to start wars? Dare to shut down coffee bean production globally and see what happens.
Coffee and tea are the most consumed drinks in the world. We’re a planet full of bean suckers and leaf lickers. The reasons we should stop consuming caffeine can be collectively counted on one middle finger. Another positive article about the joys of supporting THE global wonder drug and the multi-trillion dollar industry behind it? No shit. You don’t say. I’m shocked. Pass the beans and the grinder.
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Given the sheer amount of humans that are addicted to caffeine, are we sure we are still capable as a race to study this fairly, without obvious bias?
I think you overestimate just how much the most consumed drink in the world actually penetrantes the world. I live in one of the most coffee consuming countries in the world and I know countless people who don't drink tea or coffee. It's popular for sure, but it's not completely ubiquitous.
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And when adding in Coke/Pepsi/Redbull and co ... what's the percentage then?
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Given the sheer amount of humans that are addicted to caffeine, are we sure we are still capable as a race to study this fairly, without obvious bias?
I think you overestimate just how much the most consumed drink in the world actually penetrantes the world. I live in one of the most coffee consuming countries in the world and I know countless people who don't drink tea or coffee. It's popular for sure, but it's not completely ubiquitous.
Tea and coffee holding the top two spots merely demonstrates the undying extent we tea lickers and bean suckers will go through to feed addiction under the guise of timeless tradition.
Needless to say the Red Bull Vape Generation bent over the espresso enema bar taking double shots are on a whole new level of addiction in fashionable disguise. Looking at history, we prolly should have seen that shit coming.
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Autophagy needs both AMPK and mTOR activation (Score:2)
Amino acids (aa) are not only building blocks for proteins, but also signalling molecules, with the mammalian target of rapamycin complex 1 (mTORC1) acting as a key mediator. However, little is known about whether aa, independently of mTORC1, activate other kinases of the mTOR signalling network. To delineate aa-stimulated mTOR network dynamics, we here combine a computational–experimental approach with text mining-enhanced quantitative proteomics. We report that AMP-activated protein kinase (AMPK), phosphatidylinositide 3-kinase (PI3K) and mTOR complex 2 (mTORC2) are acutely activated by aa-readdition in an mTORC1-independent manner. AMPK activation by aa is mediated by Ca2+/calmodulin-dependent protein kinase kinase (CaMKK). In response, AMPK impinges on the autophagy regulators Unc-51-like kinase-1 (ULK1) and c-Jun. AMPK is widely recognized as an mTORC1 antagonist that is activated by starvation. We find that aa acutely activate AMPK concurrently with mTOR. We show that AMPK under aa sufficiency acts to sustain autophagy. This may be required to maintain protein homoeostasis and deliver metabolite intermediates for biosynthetic processes.
In figure 7d, you can see why both AMPK and mTOR are needed for autophagy https://www.nature.com/article... [nature.com]
Fission yeast? (Score:3)
And in related news, Iranian scientists studying fission yeast have suddenly stopped ageing.
Breaking News (Score:2)
Slashdot posts actual science, not a "study / grant request".
I'm gonna live forever! (Score:2)
That's a curse, by the way, not an exclamation of joy.
As Good A Reason As Any... (Score:2)
sleep (Score:2)
Let me guess (Score:1)
Brought to you by the coffee industry?