Bear with me for a moment to walk through a bit of the science. The conclusion is going to knock your socks off…
You already know that your cells reproduce by dividing in two. From the moment of conception until the final minutes of life, the trillions of cells in your body are regenerating through this process.
Over the course of your early years, your cells continue to divide at will with little change in overall health and longevity. This is how the growth process unfolds: your body is constantly rebuilding, repairing, and renewing itself.
What had experts stumped for decades was why cells in older folks dividing by the exact same process – started slowing down over time, eventually stopped dividing…and died.
Think about it: if the physiological process of cell division doesn’t change over your lifetime, shouldn’t new cells look and function the same regardless of your age?
But they don’t. You can tell the difference between a newly divided “old” cell and a newly divided “young” one just by looking at them under a microscope. Each new cell is not an exact copy of its parent cell. This is how we age. Still, the reason why remained a mystery.
The answer emerged slowly over the last half a century. The first breakthrough came in 1965, when a geneticist named Leonard Hayflick discovered that most cells only divide about 80 times, then slow down and die.1
This became known as the “Hayflick limit.” He proved there’s an “internal clock” that carefully ticks off the rate of division among all the trillions of cells in your body.
Not only that this mysterious clock appears to “tell” each cell when to start functioning less and less efficiently…and when to launch a “programmed” death. It’s as if your whole lifespan is repeated in miniature at the cellular level.
Hayflick’s discovery had important implications for the field of anti-aging. His work suggested that there is a mechanism inside every cell that determines longevity.
Suppose you could somehow “tinker” with this internal clock, slow it down or put on the brakes? This seemed possible at least in theory. But we still hadn’t found out exactly where the cells’ “internal clock” is or how it works.
It was finally discovered twenty-five years later. The prestigious journal Nature published a groundbreaking article in 1990 that introduced the world to an explanation of the genetic mechanism that involves something called the “telomere.”2
Telomeres are small stretches of protein “caps” at the ends of every cell’s DNA. They are represented here graphically:
DNA is made up of two “strands” of long sequences of genes. As you can see, they take the shape of what’s called a “double helix” – sort of like a spiral staircase. They contain all your genetic material.
The telomeres act like the plastic fittings at the end of your shoelaces. They were previously known only for their role in healthy gene function because they keep the ends from “fraying.”
What the authors published in Nature was the new realization that the telomere is also your biological clock. Each time your cells divide, a small end portion of the telomere is not copied making your telomeres get shorter and shorter over time. Each new generation of cells has a slightly shorter telomere than its parent did. Further research confirmed it.3 Telomeric length is now known as the marker of a given cell’s age.
And, it turned out that telomeres are more than just “counters” that tick off your cell’s age. They also govern the aging process. As they shorten with each new division, they cause the chromosome to fold differently exposing a different portion of your genome. This is how you can be so different at 72 than you were at 2. You have the same genes. But… you are transcribing or reading a different combination of genes as you age. This process eventually signals to your cells to “grow old,” stop dividing and that cell line dies off.
Later studies revealed even more promising discoveries. Researchers showed that telomeric length for certain types of cells stays the same.4 For example, some cancer cells do not lose any of their telomeres as they divide. They are technically “immortal,” and this is one of the reasons why they wreak such havoc on the body. They can keep dividing without losing any genetic material, until they finally take over.
The question remained is there a safe way that we can maintain telomere length as your cells divide over time? We now know the answer is yes.
[Ed. Note: If you're interested in receiving TA-65 or would like more information, please call my office at 561.784.7852.]
1 Hayflick L. “The limited in vitro lifetime of human diploid cell strains.” Experimental Cellular Research. 1965. 37 (3): 614-636.
2 Harley et al. “Telomeres shorten during ageing of human fibroblasts.” Nature. 1990. (345):458–460.
3 Zglinicki, T. “Telomeres influencing the rate of aging.” Annals of the New York Academy of Science. 1998. (854):318-27.
4 Reddel and Bryan. “Alternative lengthening of telomeres: dangerous road less traveled.” Lancet. 2003. 361(9372):1840-1.
5 www.tasciences.com/ta65molecule.html
6 www.tasciences.com/pattonprotocol.html
7 Xu et al. “Homocysteine accelerates endothelial cell senescence.” FEBS Letters. 2000. 470:20-24.
