Our bodies are astonishing in so many ways! But perhaps the most miraculous ability of the body is the way it is able to continually renew itself.
Your body is constantly removing damaged and/or inefficient cells (a process called autophagy). And it’s also replacing them with new cells (cell division). It is through this renewal process that even as you get older, your body stays young. It’s also why you’re able to function for so many more years than you would think possible.
Unfortunately, there’s one small problem. As you age, this renewal process starts to slow down.
Your body doesn’t replace those damaged, inefficient cells at the same rate it used to. And more and more of our cells become non-functional. This is the essence of the aging process. But isn’t there something we can do to slow all of this down? Absolutely! I’ve shown you several ways in the past. But this week, I’m going to tell you the only proven way to slow this process down.
I’ve uncovered new experimental research that explains why the renewal process slows down. And, more importantly, it shows very clearly what you can do about it.
It has to do with telomeres. I’ve told you about telomeres in the past. So you may know that a telomere is a string of repetitive DNA sequences at the end of each one of our chromosomes. It’s the tail of your chromosomes. Even though telomeres are made of DNA, the DNA they contain is not essential to cell function.
Why Are Telomeres Important?
When your cells divide and the strands of DNA split up to form two new cells, the division destroys the DNA at the very ends of the chromosomes where the telomeres are. When this happens, the telomeres become shorter. This is just a natural side effect of cell division. But since the DNA in the telomeres is not essential to cell function, their destruction doesn’t matter.
So it’s a good thing God gave us telomeres. If they weren’t there, then every time your cells divided, you would lose critical genetic material. You would very quickly come to the end of your earthly existence. But since they are there, our cells can repeatedly divide without ever losing any of their critical genetic code.
But there is one small problem. If the telomeres become shortened every time a cell divides, then what happens when they shorten to the point that they can no longer protect the chromosomes? The answer is that the cell stops dividing. It goes into what is called a phase of “senescence,” which means that its function slows down to almost zero. As our cells enter into this senescent phase, the entire body follows suit. This is the root cause of the aging process. So if it were possible to slow down telomere shortening, it would be possible to slow down aging.
And that’s exactly what this new research shows you how to do.
Are You Getting Too Much Oxygen?
In one experiment, researchers at the Humboldt University in Berlin, Germany, looked at the effects of excessive amounts of oxygen on fibroblast cells. Fibroblasts are cells that are instrumental in repairing your body after an injury.
To conduct the experiment, they grew these cells in two cultures. They exposed one culture to 21% oxygen, the same concentration found in the air we breathe. They exposed the other culture to 40% oxygen – roughly twice as much. What they discovered is remarkable.
The cells exposed to the high concentration of oxygen went into a senescence phase. Why? Because the telomeres in those cells shortened five times more with each division than the telomeres in the cells exposed to the lower concentration.
In other words, they aged five times faster!
Two Primary Ingredients to Stay Young
Now, before we can put this puzzle together, let’s look at the equally amazing results of another telomere study.
In the second study, the researchers took biopsies of the skin of 16 people between the ages of 28 and 91 years. They separated out the fibroblasts and grew them in test tubes until they had gone through at least 20 divisions. Then they measured three things.
First they measured the change in the length of the telomeres. Since the cells had undergone 20 divisions, it would stand to reason that their telomeres would have undergone some shortening. And, of course, that is exactly what they found.
Next, they measured the amount of protein carbonyls in each batch of cells. Protein carbonyls are the byproduct of cells exposed to free radical damage. The more free radical damage a cell has the more protein carbonyls it will contain.
And lastly, they measured the levels of two of the major intracellular antioxidant enzymes – glutathione peroxidase and superoxide dismutase. These enzymes protect our cells from free radical damage. What they found is extremely important.
The cells with the lowest levels of the antioxidant enzymes had the most telomere shortening. They also had the highest levels of protein carbonyls. Every case was the same. The length of the telomeres in each cell was always determined by the amount of the antioxidant enzymes in the cell.
In fact, the relationship was so close that the researchers concluded that the telomere length of a cell was an excellent way to determine how many antioxidant enzymes the cell had. This observation is proof positive that a major, if not the primary, cause for telomere shortening (and hence the aging process) is a decrease in the amount of the antioxidant enzymes glutathione peroxidase and superoxide dismutase.
How to Keep Your Telomeres Long
These studies appear to give us two different explanations for aging. But they really don’t. In fact, I’m going to show you how they work together. And I’m going to show you how to use this information to stay young.
To do that, I need to explain how your cells use oxygen.
Cells need oxygen to live. But there’s a limit to how much oxygen they can process. We call this limit a cell’s “aerobic capacity.” If a cell has a high aerobic capacity, then it can process a large amount of oxygen.
When you expose a cell to higher levels of oxygen, as long as you don’t exceed its aerobic capacity, it will thrive. But once you expose a cell to levels of oxygen that are greater than it can process (greater than its aerobic capacity), you create a problem. That problem is excessive free radical production. This happens because the cell has to do something with all that extra oxygen. And what it ends up doing is converting it into free radicals.
In study number one, the researchers exposed fibroblast cells to an excessive amount of oxygen – a level that was sure to exceed their aerobic capacity. This would have caused the cells to greatly overproduce free radicals. As a result, it dramatically shortened the telomeres. Could it be that the shortening was the result of excessive free radical production? Study number two gives us the answer.
This study showed that telomere shortening is directly related to how many free radicals a cell produces. The more free radicals a cell produces, the shorter the telomeres, and the more rapidly the cells aged.
So the common denominator that both of these studies have is that telomere shortening, and hence aging itself, comes as a direct result of excessive free radical damage to the telomeres. And what is responsible for all of this excessive free radical damage?
Study number one shows us that one cause is a decrease in aerobic capacity. Study number two tells us that it’s a result of a decreased amount of the antioxidant enzymes glutathione peroxidase and superoxide dismutase.
So how can you increase your aerobic capacity? And where can you buy these enzymes?
Let’s take the second question first. You can buy these enzymes on the Internet and most health food stores. But don’t do it. They won’t work. No matter whether you take the enzymes by mouth or inject them, they won’t work. Your body metabolizes them long before they reach the cellular level. So taking the enzymes is not an answer to our problem. So what is?
Well, we need to answer the first question to discover this secret. How can you increase your aerobic capacity?
This answer is easy. All you have to do is to exercise. But not just any kind of exercise will do. It has to be regular. That means at least every other day. And it has to be done correctly. That means it has to be done in a series of intervals in which you exceed your aerobic capacity for a brief period of time.
I’ve discussed this in the past, and these exercise guidelines are on my website. These guidelines work. I’ve tested them. And time after time, the surest way I have found to increase aerobic capacity is exercise properly done.
And, by the way, properly performed exercise has one other advantage. It is the only known way to increase your levels of glutathione peroxidase and superoxide dismutase. So you don’t have to buy anything to live longer.
By spending only 20-30 minutes, three to four times a week exercising properly, you are doing everything you need to do to maintain a healthy telomere length. And it’s free! Sounds like a good deal to me.
How to Stop the Aging Process Without Exercise
But what if you can’t exercise? What if your hip is bad or your lungs are bad? What if you are just too sick to exercise? What then?
These situations are perfect for oxidative therapy.
You have heard me talk about oxidative therapy before. I call it “exercise in a bottle.” It’s a form of medical therapy that I have been using for over 25 years. Back then, very few doctors used oxidative therapies. Today, doctors all over the world use it. Oxidative therapies have the same effects as exercise. They increase aerobic capacity, and simultaneously increase the levels of glutathione peroxidase and superoxide dismutase.
The most common forms of oxidative therapy are ozone therapy, intravenous hydrogen peroxide therapy, and exercise with oxygen therapy (EWOT). If you find yourself in a fix that prevents you from exercising like you need to, you should find a doctor versed in oxidative therapy. You can find them at www.aaot.us, www.oxygenhealingtherapies.com, and www.acam.org.
von Zglinicki, T., G. Saretzki, W. Döcke, and C. Lotze. “Mild hyperoxia shortens telomeres and inhibits proliferation of fibroblasts: a model for senescence?” Exp Cell Res. 1995 September;220(1):186-93.
Serra, V., T. Grune, N. Sitte, et al. “Telomere length as a marker of oxidative stress in primary human fibroblast cultures.” Ann N Y Acad Sci. 2000 June;908:327-30.