How Important is the Role of Telomeres in Aging?

Some long-lived species like humans have telomeres that are much shorter than species like mice, which live only a few years. Nobody knows why. But it's evidence that telomeres alone do not dictate lifespan.

Cawthon's study found that when people are divided into two groups based on telomere length, the half with longer telomeres lives an average of five years longer than those with shorter telomeres. This study suggests that lifespan could be increased five years by increasing the length of telomeres in people with shorter ones.

People with longer telomeres still experience telomere shortening as they age. How many years might be added to our lifespan by completely stopping telomere shortening? Cawthon believes 10 years and perhaps 30 years.

factors_in_aging_tnAfter age 60, the risk of death doubles every 8 years. So a 68-year-old has twice the chance of dying within a year compared with a 60-year-old. Cawthon's study found that differences in telomere length accounted for only 4% of that difference. And while intuition tells us older people have a higher risk of death, only 6% is due purely to chronological age. When telomere length, chronological age, and gender are combined (women live longer than men), those factors account for 37% of the variation in the risk of dying over age 60. So what causes the other 63%?

A major cause of aging is “oxidative stress.” It is the damage to DNA, proteins, and lipids (fats) caused by oxidants, which are highly reactive substances containing oxygen. These oxidants are produced normally when we breathe and also result from inflammation, infection, and consumption of alcohol and cigarettes. In one study, scientists exposed worms to two substances that neutralize oxidants, and the worms' lifespan increased an average 44%.

Another factor in aging is “glycation.” It happens when glucose, the main sugar we use as energy, binds to some of our DNA, proteins, and lipids, leaving them unable to do their jobs. The problem becomes worse as we get older, causing body tissues to malfunction, resulting in disease and death. Glycation may explain why studies in laboratory animals indicate that restricting calorie intake extends lifespan.

Most likely oxidative stress, glycation, telomere shortening, and chronological age — along with various genes all work together to cause aging.

telomere_length_tnTelomeres and other diseases

People with a disease named dyskeratosis congenita have telomeres that get short much more quickly than normal.

These people endure premature aging and death. They face a higher risk of life-threatening infections, leukemia and other blood cancers, intestinal disorders, cirrhosis of the liver, and pulmonary fibrosis, a deadly stiffening of lung tissue. They also are more likely to endure gray hair, balding, poor wound healing, spots on the skin, intestinal disorders, softening of the bones, and learning disabilities.

The implication is that telomeres may play a role in all those conditions because they all involve tissues in which cells divide often. There also is some evidence linking shortened telomeres to Alzheimer disease, hardening of the arteries, high blood pressure, and type 2 diabetes.

Epitalon

Longevity isn't just about living longer, but about living healthier. Studies show that Epitalon not only reactivates telomerase and thus extends a cell's life, but that it also reduces rates of DNA mutation, prevents degradation of immune function, promotes the health of the intestinal mucosa, and protects nerves from damage in rodent models. In other words, epitalon extends both lifespan and health span (the number of years without disease or disability).

You can read more about Epitalon, here, and it can be obtained, now, through OceansLab!

Epitalon_Telomerase_longevite_web-300x201


Source(s):

ncbi.nlm.nih.gov/pubmed

khavinson.info

learn.genetics.utah.edu

S. V. Rosenfeld, E. F. Togo, V. S. Mikheev, I. G. Popovich, V. K. Khavinson, and V. N. Anisimov, “Effect of epithalon on the incidence of chromosome aberrations in senescence-accelerated mice,” Bull. Exp. Biol. Med., vol. 133, no. 3, pp. 274-276, Mar. 2002.

V. K. Khavinson, E. G. Rybakina, V. V. Malinin, I. Y. Pivanovich, S. N. Shanin, and E. A. Korneva, “Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway,”Bull. Exp. Biol. Med., vol. 133, no. 5, pp. 497-499, May 2002.

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