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The Secrets of Aging Well and Living Better

Ch. 45 - Protection of Telomeres Through Diet

Chapter 45

Protection of Telomeres Through Diet

Long-term studies that tracked telomere length over time in the same individuals found, surprisingly, that in 1.5 to 25 percent of individuals, telomeres lengthened. In the Bogalusa Heart Study, for example, telomeres grew in 16 percent of all participants over a period of seven years, but by the twelfth year that number had fallen to 1.5 percent. So time probably always wins in the end, but thanks to telomere activation we might keep telomeres from shrinking year after year.

Changes in telomere length could have serious consequences for health. In the MacArthur Study of Successful Aging, for example, older men whose telomeres shortened over the course of two and a half years were three times more likely to die of cardiovascular disease in the next ten years than participants whose telomeres grew or simply stayed the same. People who live to 100 seem to be especially good at preserving their telomeres, especially those who successfully avoid major age-related diseases. So is telomerase the “fountain of youth” it has been made out to be? A “molecular switch that turns off aging”?

Mice with artificially induced telomerase deficiency suffer from critical shortening of their telomeres, premature aging, and early death, which can be prevented if their telomerase is restored. Conversely, mice astonished researchers when they were engineered to express the enzyme even more strongly, with a 40 percent longer lifespan. And further evidence of its anti-aging activity: telomerase activation in different mouse models has been shown to reduce age-related osteoporosis, improve heart, liver, and kidney function, as well as coordination, balance, and movement. Telomerase may even have additional, “noncanonical” benefits such as DNA repair.

What about cancer?

Cancer cells can hijack telomerase—so should we worry that increasing telomerase activity could raise our cancer risk? Pharmaceutical companies have tried to develop an anti-telomerase chemotherapy for cancer, but without success. Not only are there toxic effects on stem cells that depend on telomerase, but the cancer is not stopped in time. Even if telomerase were completely blocked and cancer-cell telomeres were to fray, we would be dead long before the Hayflick limit was reached. (The cancer cells produced after 50 divisions would be enough to kill us.)

Increasing telomerase activity, however, does not appear to be a problem. Telomerase can allow cancer, but it is not a sufficient trigger for it; that is, the enzyme can be used by cancer cells but is not itself the cause of the disease. Skin cells (from circumcised foreskins) were “made immortal” in a Petri dish by telomerase activation, but did not turn into skin cancer cells. Similarly, telomerase activation in mice delays aging and increases life expectancy without increasing cancer risk. Since it therefore seems to have only benefits, we should try to boost the activity of this age-defying enzyme.

Protection of Telomeres Through Diet

Genetically determined differences in the rate at which telomeres shorten account for about 30 percent in humans, but the biggest influence on whether our telomeres become longer or shorter, and at what pace, comes from external factors such as environment, lifestyle, and diet. That explains, for example, why spouses have similarly long telomeres, but it does not necessarily mean we fully control the remaining 70 percent of our telomeres’ fate. We can, for example, lose telomeres even before birth if we are exposed in the womb to alcohol, smoke, or air pollution. But the choices we make every day—or three times a day—can make a difference.

The biggest driving forces behind accelerated telomere loss are probably oxidative stress and inflammation. (How and why, see see.nf/ttaggg.) So it is not surprising that a systematic review of the role of diet found that longer telomeres are associated with eating vegetables, fruit, legumes, nuts, and other foods high in fiber and antioxidants. In contrast, consumption of processed meat, alcohol, soft drinks, and other foods and beverages high in saturated fat and sugar was associated with shorter telomeres. So a whole-food, plant-based diet was put to the test.

Turning Back the Clock

Dean Ornish, the scientific pioneer, was the first to show in a randomized controlled trial that a whole-food plant-based diet can reverse the progression of heart disease. He then showed that the same dietary changes could help halt early-stage prostate cancer, and he is currently forging plans against dementia to reverse the course of early-stage Alzheimer’s. For a study partially funded by the US Department of Defense that aimed to determine what impact healthy diet and lifestyle have on cellular aging, Ornish teamed up with Dr. Elizabeth Blackburn, who received the Nobel Prize in Medicine for her role in the discovery of telomerase.

30 men between 49 and 80 were to eat a low-fat diet that was primarily whole-food and plant-based—fruit, vegetables, whole grains, and beans. They were also to go for walks and practice stress management. Within three months, their telomerase activity jumped by almost 30 percent. This was the very first intervention ever to show a significant strengthening of the telomerase enzyme. The study was published in a world-leading medical journal, and the accompanying editorial concluded that the spectacular findings should “encourage people to live healthfully to prevent or combat cancer or age-related disease.”

In the follow-up study five years later, the scientists measured the participants’ telomere length to see whether strengthening telomerase had indeed led to a slowing of telomere loss. In the similarly aged men in the control group, who had continued eating as usual, telomeres, as expected, had shrunk with age. In the healthy-lifestyle group, however, the participants’ telomeres not only shrank less or remained stable—they grew. Five years after the first intervention, their telomeres were on average even longer than at the beginning of the study, suggesting for the first time that a healthy, plant-based diet and corresponding lifestyle can increase the activity of the telomerase enzyme and practically reverse cellular aging. But was it the diet, the exercise, or the stress management?

Can We De-Stress Our Telomeres?

In the blockbuster The Holiday, the character played by Cameron Diaz declares: “Great stress … makes the DNA in our cells shrink until they can no longer reproduce.” Did Hollywood get it right? As I explain in see.nf/destress, the data on stress and telomeres are contradictory. For example, in one group of people caring for individuals with dementia, lower telomerase activity was found, and in another, increased activity. In the video you also see that the data on the role of meditation are mixed as well. Still, there seems to be more to Ornish’s remarkable results than the stress-reduction component. What about exercise and weight loss?

Telomere Length in the Long Run

We can’t always change our location in life, but we can always take a walk in the fresh air. A study of thousands of twins found that those who exercised more seemed to strengthen not only their muscles but also their telomeres. Although some research suggests that as little as 150 minutes of walking per week is associated with longer telomeres and, on average, people who exercise tend to have longer telomeres than those who do not, the majority of studies on physical activity and telomere length actually failed to meet expectations and found no significant association. “It is not clear,” concluded one review, “whether physical activity protects against shortening of telomere DNA.”