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Volume 4 Issue 4

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The new study is a follow up to a similar, three-month pilot inves ga on in 2008 in which the same par cipants were asked to follow the same lifestyle program. A er three months, the men in the ini al study exhibited significantly increased telomerase ac vity. Telomerase is an enzyme that repairs and lengthens telomeres. The new study was designed to determine if the lifestyle changes would affect telomere length and telomerase ac vity in these men over a longer me period. "This was a breakthrough finding that needs to be confirmed by larger studies," said co-senior author Peter R. Carroll, MD, MPH, professor and chair of the UCSF Department of Urology. "Telomere shortening increases the risk of a wide variety of chronic diseases," Carroll said. "We believe that increases in telomere length may help to prevent these condi ons and perhaps even lengthen lifespan." H ow B i g I s T h e R o l e o f Te l o m e r e s i n A g i n g ? 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 s ll 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. A er 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 intui on 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 varia on in the risk of dying over age 60. So what causes the other 63%? A major cause of aging is "oxida ve stress." It is the damage to DNA, proteins, and lipids (fats) caused by oxidants, which are highly reac ve substances containing oxygen. These oxidants are produced normally when we breathe, and also result from inflamma on, infec on, and consump on of alcohol and cigare es. In one study, scien sts exposed worms to two substances that neutralize oxidants, and the worms' lifespan increased an average 44%. Another factor in aging is "glyca on." 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 ssues to malfunc on, resul ng in disease and death. Glyca on may explain why studies in laboratory animals indicate that restric ng calorie intake extends lifespan. Most likely oxida ve stress, glyca on, telomere shortening, and chronological age — along with various genes — all work together to cause aging. W h a t A r e T h e P r o s p e c t s f o r H u m a n Im m o r t a l i t y ? Human lifespan has increased considerably since the 1600s, when the average lifespan was 30 years. By 2012, the average US life expectancy was nearly 79. Reasons for the increase include sewers and other sanita on measures, an bio cs, clean water, refrigera on, vaccines and other medical efforts to prevent children and babies from dying, improved diets, and be er health care. Some scien sts predict average life expectancy will con nue to increase, although many doubt the average will ever be much higher than 90. But a few say vastly longer lifespans are possible. Cawthon says that if all processes of aging could be eliminated and oxida ve stress damage could be repaired, "one es mate is people could live 1,000 years." Abby's Magazine - Volume 4 Issue 4 | Page 41

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