Exciting Research Points to THE Way to Live Better, Longer

Dr. Frank Shallenberger, MD

November 11, 2019



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 apoptosis) and replacing them with new cells (cell division). It is through this renewal process that even as we get older, our bodies stay young, and we are able to remain functional for so many more years than one would think is possible.

Now that should make you pretty happy — except for one small problem. As we become older, this renewal process starts to slow down. Fortunately, there’s plenty you can do to rev up this renewal process.

As you age, your body doesn’t replace 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, and the weakness and frailty that comes with it. So what is it that we can do to slow all of this down?

Two experimental research papers offer significant insight into why the renewal process slows down, and more importantly, what you can do about it.

Why Our Body Slows Down With Age

But before I can tell you about this exciting research, I need to explain why the process of cellular division stops as we get older. It has to do with telomeres. Now, you may already know about telomeres. If you do, then please forgive the brief explanation.

A telomere is a string of repetitive DNA sequences at the end of each one of our chromosomes. Even though telomeres are made of DNA, the DNA they contain is not essential to cell function. And here’s why that’s 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. At the same time, it shortens the length of the telomeres. 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 that the Creator gave us telomeres. Because if they weren’t there, then every time our cells divided, we would lose critical genetic material, and very quickly come to the end of our earthly existence. But since they are there, our cells can repeatedly divide without ever losing any of our genetic code.

But there is one small problem that maybe some of you have thought of. 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 just stops dividing. It goes into what is called a phase of senescence. This means that its function slows down to almost zero. And, as all of 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 these research papers are showing us how to do.

Research Proves You Can Slow Aging

In one experiment, conducted at the Humboldt University in Berlin, Germany, the researchers looked at the effects of excessive amounts of oxygen on fibroblast cells. Fibroblasts are cells that are instrumental in repairing our bodies after an injury.

The researchers grew these cells in two cultures. They exposed one culture to 21% oxygen, the same concentration in the air we breathe. The other culture they exposed to 40% oxygen – roughly twice as much. What they discovered was 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! Now, before we 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 from the biopsies. They grew the fibroblasts in test tubes until they had gone through at least 20 divisions. Then they measured three things.

The first thing they measured was 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 form when cells have free-radical damage. The more free-radical damage that 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. Here’s what the researchers found.

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 amount of the antioxidant enzymes in the cell always determined the length of the telomeres in each 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 major cause for telomere shortening (and hence the aging process) is a decrease in the amount of the antioxidant enzymes glutathione peroxidase and superoxide dismutase.

What This Means for You

So now, let’s put these two studies together, and see what adds up.

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. What happened as a result was it dramatically shortened the telomeres of these cells. Could it be that the shortening occurred because of excessive free-radical production? Let’s look at study number two.

This study showed that telomere shortening was directly related to the production of free radicals. The more free radicals your body produces, the shorter the telomeres, and the more rapidly your cells age.

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 causes this excessive 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 anti-oxidant enzymes glutathione peroxidase and superoxide dismutase. So I know the next thing you are already thinking.

How can I increase my aerobic capacity, and where can I buy these enzymes?

Let’s take the second question first. The answer is you can buy these enzymes on the Internet. But the problem is that 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. Now let’s take the first question. How can I increase my aerobic capacity?

This answer is easy. All you have to do is to exercise. But not just any old kind of exercise will do. It has to be regular (at least every other day). And you have to do it correctly. That means it has to be done in a series of intervals in which you exceed your aerobic capacity for a brief period.

I’ve published my exercise guidelines in the past, which you can find on my website. And I know they work, because I have tested them. As I talked about before, Bio-Energy Testing measures aerobic capacity. I have performed over 3,500 tests in patients of all ages, and in all conditions. And time after time, the surest way I have found to increase aerobic capacity is exercise done properly.

Oh, and by the way, properly performed exercise has one other advantage. Other than oxidative therapy, it’s the only known way to increase your levels of glutathione peroxidase and superoxide dismutase. But unlike oxidative therapy, it’s free. And you don’t have to go to a doctor's office to get it.

So let’s add it up. 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.

Two More Things to Consider

The first is to start exercising early in your life. An optimal time would be your 40th birthday. This is because my studies have shown me that it’s around this time of life that aerobic capacity starts to decrease in most people. Also, keep in mind that this process of telomere shortening is going to happen no matter what you do. Exercise just slows it down. So the earlier you start it, the more effect it will have.

What if you can’t exercise?

The other thing has to do with oxidative therapy. What if you are reading this article and 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. And other doctors all over the world use it as well. 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 intravenous ozone therapy, intravenous hydrogen peroxide therapy, and exercising 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. Good referral sites are www.oxygenhealingtherapies.com and www.acam.org.


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.

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.

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