Have Scientists Discovered An ‘On/Off’ Switch To Younger Bones?

Vivian Goldschmidt, MA Nutrition

Evidence-Based
4 min Read

Today I’ll share with you a study that provides fascinating insights into the mechanism of aging and its association with bone loss. Researchers at the University of Pennsylvania have uncovered significant breakthroughs in the realm of age-related bone loss which provides valuable information on how to keep your bones “young”.

Eternal Youth?

In the Osteoporosis Reversal Program, I point out the fact that aging is not a disease; it’s a natural biological process. Bone density naturally decreases a bit with age, but bone renewal and regeneration continues no matter your age, if you’re doing what’s right for your bones.

This is important to understand so you can confidently stand up to the Medical Establishment that sees aging and osteoporosis as “diseases”, and “treats” them as such by prescribing toxic drugs.

Now let’s take a look at the aging process, starting with our DNA.

The DNA of Aging

Just what happens at the molecular level when we age? Each double-helix-shaped molecule of our DNA has tips, and these tips have pairs of enzymes that form chains. These enzyme chains are called telomeres, and their role is fascinating.

You see, when cells regenerate and replicate (as when your body builds bone), DNA molecules must make exact copies of themselves. Telomeres help offset the inevitable misalignments that occur when DNA replicates, thereby preventing the loss of precious DNA information.

Yet in some body tissues and cells, including bone-building osteoblasts, the telomeres chains get shorter, resulting in errors in the DNA sequence as the cells replace themselves. Eventually, the telomeres chains get so short that the cell stops dividing and dies. This process can reduce the osteoblast population.

A Telomeres ‘On/Off Switch'

The University of Pennsylvania study I mentioned earlier reveals that an enzyme, called telomerase, can prevent certain cells from declining, including osteoblasts and their precursors.1 It does this by lengthening the telomeres chains, so cells can replicate normally. (Remember, it’s the shortening of the telomeres chains that eventually cause the cell to die.)

When telomeres were artificially shortened in mice via a designed lack of telomerase, age-related problems manifested, such as osteoporosis, diabetes, and neurodegeneration. These mice also died young.

While the normal aging process leads to shortened telomeres in the body, and therefore, also affecting bones, the good news is that this is not inevitable. In fact, studies have shown that a diet rich in fruits and vegetables and low in processed foods increases telomerase activity by double digits.2 Exercising and stress reduction techniques also showed beneficial effects.2 So if you’re following the Osteoporosis Reversal Program, you are already on the right track!

Easy Ways to Manage Telomerase

It may sound too good to be true, but there is scientific proof that resveratrol, a compound found in dark-skinned fruits such as grapes and blueberries, effectively increases telomerase levels.3

Aerobic activity, including walking, and taking Vitamin C, a Foundation Supplement, are also effective and easy ways to maintain desirable telomerase levels.4

Isn't it great to know that this is yet one more aspect of your bone health you can easily control without dangerous and toxic drugs?

Till next time,

References

1 Pignolo, RJ, et al. “Defects in telomere maintenance molecules impair osteoblast differentiation and promote osteoporosis.” Aging Cell. 2008 Jan; 7(1):23-31. Epub 2007 Nov 20.
2 Dean Ornish et al. “Increased telomerase activity and comprehensive lifestyle changes: a pilot study.” The Lancet Oncology. OnlineSeptember 16, 2008.
3 WANG Xiao-bin et al. “Resveratrol-induced augmentation of telomerase activity delays senescence of endothelial progenitor cells.” Chin Med J 2011;124(24):4310-4315.
4 Furumoto K et al. “Age-dependent telomere shortening is slowed down by enrichment of vitamin C via suppression of oxidative stress. Life Sci. 1998;63(11):935-48.