Transcript: Why Do We Age?
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 lengthening 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 named TOR, which stands for “target of rapamycin,” which may be a master determinant of lifespan and aging. The action of TOR has been described as the engine of a speeding 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, 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 down 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, slows down cell division and kicks in a process called autophagy, from the Greek auto meaning self, 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 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 diet 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.
To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Ariel Levitsky.
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