A bacteria discovered on Easter Island may hold the key to the proverbial fountain of youth by producing rapamycin, which inhibits the engine-of-aging enzyme TOR.
Why Do We Age?
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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
It sounds like science fiction. A bacteria in a vial of dirt, taken from a mysterious island, creating a compound that prolongs life—and, not in the traditional medical sense. Thanks to advances in modern medicine, we are living longer. But, we’re doing it by “lengthen[ing] the morbidity phase.” In other words, we live longer, but sicker, lives.
We used to die here. But, thanks to medical intervention, we now die here. “So, traditional medicine increases [the] number of old people in bad health.” Ideally, though, we’d extend lifespan by slowing aging to delay the onset of deterioration.
And that’s what this appears to do. They called it rapamycin—named after Easter Island, known locally as Rapa Nui. It inhibits an enzyme they called TOR, which stands for “target of rapamycin,” which may be a “master determinant of lifespan and ageing.” The action of TOR has been described as the engine of a “[s]peeding car without brakes.”
Rather than thinking of aging as slowly rusting, a better analogy may be “a speeding car that enters [the] low-speed zone of adulthood and damages itself because it does not and cannot slow down.” Why don’t living organisms have brakes? Because they’ve never needed them. “In the wild, [animals don’t] live long enough to experience aging.” Most die before they even reach adulthood. Just a few centuries ago, “life expectancy [in London] was less than 16 years [old].”
“Therefore, living beings need to grow as fast as possible to start reproduction before [they die] from external causes. The best evolutionary strategy may be to run at full speed. But, once we pass the finish line, once we win the race to pass on our genes, we’re still careening forward at an unsustainable pace—thanks to this enzyme TOR, which in our childhood is an engine of growth, but in adulthood can be thought of as the engine of aging. “Nature simply selects for the brightest flame, which in turn casts the darkest shadow.”
Sometimes, though, in our youth, even in our youth, our bodies need to turn down the heat. When we were evolving, there were no grocery stores; periodic famine was the norm. And so, sometimes even young people had to slow, or they might never even make it to reproductive age. So, we did evolve one braking mechanism. The way caloric restriction extends lifespan appears to be mainly through the inhibition of TOR.
When food is abundant, TOR activity goes up, prompting the cells in our body to divide. When TOR detects that food is scarce, it shifts the body into conservation mode, slowing down cell division, and kicks in a process called “autophagy”—from the Greek auto, meaning self, [and] phagy, meaning to eat; autophagy: eating one’s self. Our body realizes there isn’t much food around, and starts rummaging through our cells, looking for anything we don’t need. Defective proteins, malfunctioning mitochondria—stuff that isn’t working any more—and our body cleans house. Clears out all the junk, and recycles it into fuel, or new building materials, renewing our cells.
So, caloric restriction has been heralded as a fountain of youth. The potential health and longevity benefits of such a dietary regimen may be numerous, but symptoms may include dropping our blood pressure too low, “loss of libido, menstrual irregularities, infertility, [loss of bone], cold sensitivity, loss of strength, slower wound healing, and psychological conditions such as depression, emotional deadening, and irritability.” And, you walk around starving all the time. There’s got to be a better way, which I’ll cover in my next video.
Please consider volunteering to help out on the site.
- R Zoncu, A Efeyan, D M Sabatini. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol. 2011 12(1):21 - 35.
- M V Blagosklonny. Aging is not programmed: genetic pseudo-program is a shadow of developmental growth. Cell Cycle. 2013 12(24):1–7.
- S C Johnson, P S Rabinovitch, M Kaeberlein. mTOR is a key modulator of ageing and age-related disease. Nature. 2013 493(7432):338 - 345.
- M V Blagosklonny. Why human lifespan is rapidly increasing: Solving longevity riddle with revealed-slow-aging hypothesis. Aging (Albany NY). 2010 2(4):177 - 182.
- M V Blagosklonny. TOR-driven aging: Speeding car without brakes. Cell Cycle. 2009 8(24):4055 - 4059.
- L Fontana, T E Meyer, S Klein, J O Holloszy. Long-term low-calorie low-protein vegan diet and endurance exercise are associated with low cardiometabolic risk. Rejuvenation Res 2007. 10(2):225 - 234.
- B A Dar, M A Dar, S. Bashir. Calorie Restriction the Fountain of Youth. Food Nutr Sci. 2012 3(11):1522 - 1526.
- R Pallavi, M Giorgio, P G Pelicci. Insights into the beneficial effect of caloric/ dietary restriction for a healthy and prolonged life. Front Physiol. 2012 3:318.
- A J Dirks, C Leeuwenburgh. Caloric restriction in humans: potential pitfalls and health concerns. Mech Ageing Dev. 2006 127(1):1 - 7.
- C Vézina, A Kudelski, SN Sehgal. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. J Antibiot (Tokyo). 1975 28(10):721 - 726.
Image thanks to Hhooper1 via Wikimedia
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
It sounds like science fiction. A bacteria in a vial of dirt, taken from a mysterious island, creating a compound that prolongs life—and, not in the traditional medical sense. Thanks to advances in modern medicine, we are living longer. But, we’re doing it by “lengthen[ing] the morbidity phase.” In other words, we live longer, but sicker, lives.
We used to die here. But, thanks to medical intervention, we now die here. “So, traditional medicine increases [the] number of old people in bad health.” Ideally, though, we’d extend lifespan by slowing aging to delay the onset of deterioration.
And that’s what this appears to do. They called it rapamycin—named after Easter Island, known locally as Rapa Nui. It inhibits an enzyme they called TOR, which stands for “target of rapamycin,” which may be a “master determinant of lifespan and ageing.” The action of TOR has been described as the engine of a “[s]peeding car without brakes.”
Rather than thinking of aging as slowly rusting, a better analogy may be “a speeding car that enters [the] low-speed zone of adulthood and damages itself because it does not and cannot slow down.” Why don’t living organisms have brakes? Because they’ve never needed them. “In the wild, [animals don’t] live long enough to experience aging.” Most die before they even reach adulthood. Just a few centuries ago, “life expectancy [in London] was less than 16 years [old].”
“Therefore, living beings need to grow as fast as possible to start reproduction before [they die] from external causes. The best evolutionary strategy may be to run at full speed. But, once we pass the finish line, once we win the race to pass on our genes, we’re still careening forward at an unsustainable pace—thanks to this enzyme TOR, which in our childhood is an engine of growth, but in adulthood can be thought of as the engine of aging. “Nature simply selects for the brightest flame, which in turn casts the darkest shadow.”
Sometimes, though, in our youth, even in our youth, our bodies need to turn down the heat. When we were evolving, there were no grocery stores; periodic famine was the norm. And so, sometimes even young people had to slow, or they might never even make it to reproductive age. So, we did evolve one braking mechanism. The way caloric restriction extends lifespan appears to be mainly through the inhibition of TOR.
When food is abundant, TOR activity goes up, prompting the cells in our body to divide. When TOR detects that food is scarce, it shifts the body into conservation mode, slowing down cell division, and kicks in a process called “autophagy”—from the Greek auto, meaning self, [and] phagy, meaning to eat; autophagy: eating one’s self. Our body realizes there isn’t much food around, and starts rummaging through our cells, looking for anything we don’t need. Defective proteins, malfunctioning mitochondria—stuff that isn’t working any more—and our body cleans house. Clears out all the junk, and recycles it into fuel, or new building materials, renewing our cells.
So, caloric restriction has been heralded as a fountain of youth. The potential health and longevity benefits of such a dietary regimen may be numerous, but symptoms may include dropping our blood pressure too low, “loss of libido, menstrual irregularities, infertility, [loss of bone], cold sensitivity, loss of strength, slower wound healing, and psychological conditions such as depression, emotional deadening, and irritability.” And, you walk around starving all the time. There’s got to be a better way, which I’ll cover in my next video.
Please consider volunteering to help out on the site.
- R Zoncu, A Efeyan, D M Sabatini. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol. 2011 12(1):21 - 35.
- M V Blagosklonny. Aging is not programmed: genetic pseudo-program is a shadow of developmental growth. Cell Cycle. 2013 12(24):1–7.
- S C Johnson, P S Rabinovitch, M Kaeberlein. mTOR is a key modulator of ageing and age-related disease. Nature. 2013 493(7432):338 - 345.
- M V Blagosklonny. Why human lifespan is rapidly increasing: Solving longevity riddle with revealed-slow-aging hypothesis. Aging (Albany NY). 2010 2(4):177 - 182.
- M V Blagosklonny. TOR-driven aging: Speeding car without brakes. Cell Cycle. 2009 8(24):4055 - 4059.
- L Fontana, T E Meyer, S Klein, J O Holloszy. Long-term low-calorie low-protein vegan diet and endurance exercise are associated with low cardiometabolic risk. Rejuvenation Res 2007. 10(2):225 - 234.
- B A Dar, M A Dar, S. Bashir. Calorie Restriction the Fountain of Youth. Food Nutr Sci. 2012 3(11):1522 - 1526.
- R Pallavi, M Giorgio, P G Pelicci. Insights into the beneficial effect of caloric/ dietary restriction for a healthy and prolonged life. Front Physiol. 2012 3:318.
- A J Dirks, C Leeuwenburgh. Caloric restriction in humans: potential pitfalls and health concerns. Mech Ageing Dev. 2006 127(1):1 - 7.
- C Vézina, A Kudelski, SN Sehgal. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. J Antibiot (Tokyo). 1975 28(10):721 - 726.
Image thanks to Hhooper1 via Wikimedia
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Why Do We Age?
LicenseCreative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Content URLDoctor's Note
Sadly, Americans are Living Longer but Sicker Lives. How do we lower the activity of the aging enzyme, without caloric restriction? See my follow-up video: Caloric Restriction vs. Animal Protein Restriction.
If you’d like to see my latest DVD (all proceeds to charity), it’s available for instant download.
More tips for preserving youthful health:
- How to Slow Brain Aging by Two Years
- Dietary Prevention of Age-Related Macular Degeneration
- Boosting Immunity through Diet
- Preventing Wrinkles with Diet
- Standing Up for Your Health
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