Save Your Telomeres

Since their discovery more than 75 years ago by the Nobel Laureate geneticist Hermann Müller, telomeres have attracted worldwide attention among scientists investigating the aging process.

Telomeres are the protective caps on the ends of chromosomes composed of short DNA sequences protecting our DNA and genetic material from damage. Another Nobel Laureate, Elizabeth Blackburn, likened telomeres to the little plastic caps on the ends of shoelaces (aglets).

Under normal conditions, when a cell divides, telomeres shorten. If they grow too short, they reach what’s known as the Hayflick limit (named after the esteemed gerontologist Leonard Hayflick), and the protective capacity of the telomere decreases. Real-world relevance of telomere shortening can be observed during the aging process in humans when comparing the length of telomeres from newborns (8,000 base pairs) to adults (3,000 base pairs) to elderly individuals (1,500 base pairs).

Therefore, because several disease states and pathological processes have been linked to telomere shortening, several academic laboratories and companies have explored intervention strategies to slow down the rate of telomere attrition.

Several lifestyle factors can also significantly affect telomere health and the rate of telomere shortening. Among the most studied factors associated with shorter telomeres are psychosocial: depression, anxiety, and childhood adversity (1,2). Other lifestyle factors associated with telomere length include smoking, physical activity, drugs and toxins, and oxidative stress. Indeed, the decades of research implicating oxidative stress in the aging process has recently begun addressing and demonstrating a similarly deleterious role of oxidative stress on telomere length (3-5). As a result, antioxidant intake and subsequent plasma concentrations may be newly emerging biomarkers of telomere status (6-8).

Oxidative stress is defined as an overabundance of reactive oxygen species (ROS). Excessive oxidative stress damages DNA, proteins, and lipids. While ROS are produced under normal conditions, oxidative stress occurs under conditions of poor health. To prevent oxidative stress, the body requires antioxidant nutrients such as glutathione precursors like the amino acid cysteine (found in IsaLean® Shakes) along with specific enzymes (9,10). Among these antioxidant enzymes is catalase, which functions to convert toxic and DNA-damaging hydrogen peroxide (H2O2) into water (11,12).

With this is mind, Isagenix partnered with scientists in the School of Nutrition and Health Promotion at Arizona State University to conduct a clinical evaluation in an independent, randomized, placebo-controlled, double-blinded study to evaluate Product B’s effect on catalase and other enzymes. Third-generation Product B contains a proprietary blend of plant botanicals, antioxidants, and other bioactives that provide significant protection against telomere shortening in cellular systems.

However, obtaining clinical support as a potential natural product against telomere shortening proved difficult due to analytical shortcomings and methodological issues in measuring telomere length. For this reason most studies considering the impact of dietary, environmental, or lifestyle factors on telomeres are frequently observed in studies with thousands of study participants.

In this study researchers had subjects consume either Product B or a placebo for 12 weeks and observed that subjects supplemented with Product B demonstrated a significant elevation of catalase in red blood cells (increase by 30 percent vs. placebo). Considering the role catalase may play in the aging process, this was very exciting news and the relevance of this finding was not lost on the researchers, who commented, “The increase in catalase observed by Product B is an exciting development considering the relationship between the enzyme and increased lifespan in animal studies.”

Now, Isagenix has developed fourth generation Product B® IsaGenesis®, which contains a novel lipid-soluble blend to increase absorption and bioavailability.

Clinical and experimental evidence is slowly emerging supporting the benefits of the nutritional antioxidants, plant botanicals, and other bioactives provided by Ageless Essentials™ Daily Pack, containing Product B IsaGenesis, IsaOmega Supreme®C-Lyte®Essentials for Men™ or Essentials for Women™, and Ageless Actives™.

In conjunction with a healthy diet, weight and stress management, quality and sufficient sleep, and regular exercise, Product B IsaGenesis may provide the most optimal protection against age-accelerated telomere shortening and a longer, healthier life.

Source: isagenixhealth.net

IsaGenesis: Plant-Based Ingredients for Youthful Aging

Aging is an inevitable part of life, but how you age is something you can exert some control over.

From regular physical activity to nourishing and caring for your body, healthy choices can play a beneficial role in the aging process. Beyond a healthy lifestyle, research has pinpointed specific herbs and nutrients that can support more youthful aging, specifically through the protection of your telomeres.

What Are Telomeres?

Telomeres are the protective DNA sequences at the end of each chromosome. They are essential to maintaining genome stability within the cells, and researchers have honed in on telomeres as a marker of biological aging.

Over time, our telomeres begin to gradually shorten, which is naturally associated with normal aging. Early telomere shortening is linked to lifestyle factors such as poor diet, stress, and exposure to environmental toxins, which can lead to negative consequences for health (1-5).

Think of telomeres like the plastic caps on the end of your shoelaces. With time, they will inevitably get worn down. If you take care of your shoes, you can protect your shoelaces from splitting and fraying faster than they naturally would.

Why IsaGenesis?

A growing body of scientific literature suggests that antioxidant nutrients along with select plant extracts and herbal ingredients can support telomeres and defend against the harmful effects of oxidative stress known to accelerate the cellular aging process (6).

For those wishing to maintain a youthful energy and vitality, IsaGenesis® provides a unique blend of antioxidants and phytonutrient-rich herbal ingredients. These ingredients reinforce the body’s own defenses against oxidative stress and free radicals that can accelerate the effects of aging.

  1. Milk thistle — Milk thistle contains compounds including silymarin with demonstrated liver-supporting and free-radical defense properties (6-8).
  2. Ashwagandha — This popular herb has been used for centuries in Ayurvedic medicine and is known for its benefits in supporting the body’s ability to adapt to stress (9, 10).
  3. Horny goat weed —This botanical ingredient supports healthy aging through different mechanisms, including support for immune and endocrine systems and benefits for metabolism and organ function (11-16).
  4. Grape seed extract — Grape seed extract has a high concentration of polyphenol flavonoids, which have been shown to support parameters related to heart health and normal platelet function (17-21).
  5. Turmeric — This popular curry spice contains curcumin and other related curcuminoid phytonutrients that have benefits for brain and immune health along with support free radical defenses in the body (22, 23).
  6. Giant knotweed — Giant knotweed is a natural source of the potent phytonutrient resveratrol, also found in red wine, that provides and immune system support and has been linked with benefits for healthy aging (24-26).
  7. Pomegranate — This fruit has significant beneficial properties related to its natural polyphenol content. It has been linked to benefits for heart health, metabolism, and detoxification systems (27-29).
  8. White, green, and black tea — Various types of tea leaves contain biologically active compounds associated with many health benefits, including support for cognitive function and the circulatory system (30-33).
  9. Asian ginseng — Shown to help support normal metabolism and circulation as well as healthy immune response (34, 35).
  10. Bilberry — Provides support for cognitive function and the brain’s response to oxidative stress (36-41).

Additionally, vitamin C (ascorbic acid) and B12 (as a mix of methylcobalamin and cyanocobalamin) help combat oxidative stress and support normal metabolism. Vitamin C plays a role in developing and maintaining a healthy antioxidant status (42, 43). Adequate vitamin B12 is essential to maintain normal blood homocysteine levels. Elevated blood homocysteine is a known risk factor for oxidative stress (44, 45).

IsaGenesis Proven Effective Through Research

Catalase is a powerful protective enzyme naturally produced by cells that is key to defending against cellular damage caused by harmful, free-radical generating peroxides. Supporting the body’s defense against oxidative stress helps maintain normal telomere function and mitigates many of the factors that contribute to premature telomere shortening (1-5).

In a double-blind, randomized, placebo-controlled trial, researchers observed a 15% increase in catalase levels in participants who supplemented with IsaGenesis, compared to participants who received a placebo.

This clinical trial demonstrates that IsaGenesis supports the body’s natural defense against oxidative stress by significantly increasing catalase levels in healthy adults.

How To Use IsaGenesis

The unique blend of ingredients in IsaGenesis naturally lend itself to supporting healthy aging. But, IsaGenesis is not just for older adults. The herbal and plant-based ingredients found in IsaGenesis are beneficial for many functions of health and wellness and recommended for anyone over the age 18.

Taking two IsaGenesis capsules twice daily or as part of the Complete Essentials™ Daily Packs With IsaGenesis is the best way to provide your body with this blend of ingredients you can’t find anywhere else.

References

  1. Bull CF et al. Telomere length in lymphocytes of older South Australian men may be inversely associated with plasma homocysteine. Rejuvenation Res 2009;12:341-9.
  2. Freitas-Simoes TM, Ros E, Sala-Vila A. Nutrients, foods, dietary patterns and telomere length: Update of epidemiological studies and randomized trials. Metabolism. 2016 Apr;65(4):406-15.
  3. Wolkowitz OM et al. Leukocyte Telomere Length in Major Depression: Correlations with Chronicity, Inflammation and Oxidative Stress-Preliminary Findings. PLoS One 2011; 6(3):e17837.
  4. Cassidy A et al. Associations between diet, lifestyle factors, and telomere length in women. Am J Clin Nutr 2010;91:1273-80.
  5. Demissie S et al. Insulin resistance, oxidative stress, hypertension, and leukocyte telomere length in men from the Framingham Heart Study. Aging Cell 2006; 5: 325-30.
  6. Sweazea KL, Johnston CS, Knurick J, Bliss CD. Plant-Based Nutraceutical Increases Plasma Catalase Activity in Healthy Participants: A Small Double-Blind, Randomized, Placebo-Controlled, Proof of Concept Trial. J Diet Suppl 2016;0,0:1-14.
  7. Velussi M et al. Long-term (12 months) treatment with an anti-oxidant drug (silymarin) is effective on hyperinsulinemia, exogenous insulin need and malondialdehyde levels in cirrhotic diabetic patients. J Hepatol 1997;26:871-9.
  8. Soto C et al. Silymarin increases antioxidant enzymes in alloxan-induced diabetes in rat pancreas. Comp. Biochem. Physiol. C Toxicol. Pharmacol 2003;136:205–212.
  9. Williamson E. Withania somnifera (L.) Dunal (Solanaceae) In: Major Herbs of Ayurveda. Churchill Livingstone; 2002, 321-325.
  10. Edwards, S., I. da Costa-Rocha, E.M. Williamson and M. Heinrich, Withania somnifera (L.) Dunal (Solanaceae) Phytopharmacy – an evidence-based guide to herbal medicines. Wiley, Chichester, 2015, 32-35.
  11. Cooley K et al. Naturopathic care for anxiety: a randomized controlled trial ISRCTN78958974. PLoS One 2009;4:e6628.
  12. Wu et al. Effect of wolfberry fruit and Epimedium on DNA synthesis of the aging-youth 2BS fusion cells. Zhongguo Zhong Xi Yi Hie He Za Zhi 2003:23;926-928.
  13. Liu et al. Study on the changes of protein phosphorylation of p65 in lymphocytes of rats in progress of aging and interventional effect of Epimedium flavonoids. China Journal of Chinese Materia Medica 2008;33:73-76.
  14. Meng et al. Studies on the effect of active constituents of Herba Epimedii on hypothalamic monoamines neurotransmitter and other brain functions in aging rats. China Journal of Chinese Materia Medica 1996;21:683-685.
  15. Wang et al. Effect of Herba Epimedii and Fructus Lyciion mitochondrial DNA deletion, activity of respiratory chain enzyme complexes and ATP synthesis in aged rats. Journal of Peking University (Health Sci) 1996;21:683-685.
  16. Zeng et al. Studies on the antioxidant effect of constituents of Herba Epimedii. China Journal of Chinese Materia Medica 1997;22:46-47.
  17. Niu et al. Study on the savaging activity of Epimedii on hydroxyl radical. Chinese Journal of Sports Medicine;19:434-435.
  18. Vigna GB et al. Effect of a standardized grape seed extract on low-density lipoprotein susceptibility to oxidation in heavy smokers. Metabolism 2003; 52:1250-7.
  19. Kar P et al. Effects of grape seed extract in Type 2 diabetic subjects at high cardiovascular risk: a double blind randomized placebo controlled trial examining metabolic markers, vascular tone, inflammation, oxidative stress and insulin sensitivity. Diabet Med 2009;26:526-31.
  20. Barona J et al. Grape polyphenols reduce blood pressure and increase flow-mediated vasodilation in men with metabolic syndrome. J Nutr 2012;142:1626-32.
  21. Tome-Carneiro J et al. Consumption of a grape extract supplement containing resveratrol decreases oxidized LDL and ApoB in patients undergoing primary prevention of cardiovascular disease: a triple-blind, 6-month follow-up, placebo-controlled, randomized trial. Mol Nutr Food Res 2012;56:810-21.
  22. Weseler AR et al. Pleiotropic benefit of monomeric and oligomeric flavanols on vascular health–a randomized controlled clinical pilot study. PLos One 2011;6:328460.
  23. Nelson SK et al. The induction of human superoxide dismutase and catalase in vivo: a fundamentally new approach to antioxidant therapy. Free Radic Biol Med 2006;40:341-7.
  24. Pungcharoenkul K and Thongnopnua P. Effect of different curcuminoid supplement dosages on total in vivo antioxidant capacity and cholesterol levels of healthy human subjects. Phytother Res 2011;25:1721-6.
  25. Xia L et al. Resveratrol reduces endothelial progenitor cells senescence through augmentation of telomerase activity by Akt-dependent mechanisms. Br J Pharmacol 2008;155:387-94.
  26. Timmers S et al. Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans. Cell Metab 2011;14:612-22.
  27. Brasnyo P et al. Resveratrol improves insulin sensitivity, reduces oxidative stress and activates the Akt pathway in type 2 diabetic patients. Br J Nutr 2011;106:383-9.
  28. Rosenblat M et al. Anti-oxidative effects of pomegranate juice (PJ) consumption by diabetic patients on serum and on macrophages. Atherosclerosis 2006;187:363-71.
  29. Heber D et al. Safety and antioxidant activity of a pomegranate ellagitannin-enriched polyphenol dietary supplement in overweight individuals with increased waist size. J Agr Food Chem 2007;55:10050-4.
  30. Guo C et al. Pomegranate juice is potentially better than apple juice in improving antioxidant function in elderly subjects. Nutr Res 2008;28:72-7.
  31. Scholey A et al. Acute neurocognitive effects of epigallocatechin gallate (EGCG). Appetite 2012;58:767-70.
  32. Wightman EL et al. Epigallocatechin gallate, cerebral blood flow parameters, cognitive performance and mood in healthy humans: a double-blind, placebo-controlled, crossover investigation. Hum Psychopharmacol 2012;27:177-86
  33. Kuriyama S et al. Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project 1. Am J Clin Nutr 2006;83:355-61.
  34. Mandel SA et al. Molecular mechanisms of the neuroprotective/neurorescue action of multi-target green tea polyphenols. Front Biosci 2012;4:581-98.
  35. Ramesh T, Kim SW, Hwang SY, Sohn SH, Yoo SK, Kim SK. Panax ginseng reduces oxidative stress and restores antioxidant capacity in aged rats. Nutr Res 2012;32:718-26.
  36. Shergis JL, Zhang AL, Zhou W, Xue CC. Panax ginseng in Randomised Controlled Trials: A Systematic Review. Phytother Res 2012.
  37. Krikorian R, Shidler MD, Nash TA et al. Blueberry supplementation improves memory in older adults. J Agric Food Chem 2010;58:3996-4000.
  38. Joseph JA, Shukitt-Hale B, Willis LM. Grape juice, berries, and walnuts affect brain aging and behavior. J Nutr 2009;139:1813S-7S.
  39. Williams CM, El Mohsen MA, Vauzour D et al. Blueberry-induced changes in spatial working memory correlate with changes in hippocampal CREB phosphorylation and brain-derived neurotrophic factor (BDNF) levels. Free Radic Biol Med 2008;45:295-305.
  40. Legault J, Girard-Lalancette K, Grenon C, Dussault C, Pichette A. Antioxidant activity, inhibition of nitric oxide overproduction, and in vitro antiproliferative effect of maple sap and syrup from Acer saccharum. J Med Food 2010;13:460-8.
  41. Brewer GJ, Torricelli JR, Lindsey AL et al. Age-related toxicity of amyloid-beta associated with increased pERK and pCREB in primary hippocampal neurons: reversal by blueberry extract. J Nutr Biochem 2009.
  42. Dulebohn RV, Yi W, Srivastava A, Akoh CC, Krewer G, Fischer JG. Effects of blueberry (Vaccinium ashei) on DNA damage, lipid peroxidation, and phase II enzyme activities in rats. J Agric Food Chem 2008;56:11700-6.
  43. Groff and Gropper. Advanced Nutrition and Human Metabolism. 5th Ed. Belmont, CA: Wadsworth Learning. 2000.
  44. Shils et al. Modern Nutrition in Health and Disease. 10th Ed. 2009.
  45. Fenech M et al. Folate, vitamin B12, homocysteine status and DNA damage in young Australian adults. Carcinogenesis 1998; 19: 1163-71.

Source: isagenixhealth.net

Are Telomeres the Key to Aging and Cancer

Fluorescence-stained chromosomes (red) on a microscope slide. Telomeres (yellow) sit at the ends of each chromosome. Photo courtesy of Dr. Robert Moyzis, UC Irvine, US Human Genome Program
Fluorescence-stained chromosomes (red) on a microscope slide. Telomeres (yellow) sit at the ends of each chromosome. Photo courtesy of Dr. Robert Moyzis, UC Irvine, US Human Genome Program

Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.

Telomeres have been compared with the plastic tips on shoelaces because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism’s genetic information.

Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or “senescent” or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.

What Are Telomeres?

Like the rest of a chromosome, including its genes, telomeres are sequences of DNA — chains of chemical code. Like all DNA, they are made of four nucleic acid bases: G for guanine, A for adenine, T for thymine, and C for cytosine.

Telomeres are made of repeating sequences of TTAGGG on one strand paired with AATCCC on the other strand. Thus, one section of telomere is a “repeat” made of six “base pairs.”

In white blood cells, the length of telomeres ranges from 8,000 base pairs in newborns to 3,000 base pairs in adults and as low as 1,500 in elderly people. (An entire chromosome has about 150 million base pairs.) Each time it divides, an average cell loses 30 to 200 base pairs from the ends of its telomeres.

Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent or die.

Telomeres do not shorten in tissues where cells do not continually divide, such as heart muscle.

Why do chromosomes have telomeres?

Without telomeres, the main part of the chromosome — the part with genes essential for life — would get shorter each time a cell divides. So telomeres allow cells to divide without losing genes. Cell division is necessary for growing new skin, blood, bone, and other cells.

Without telomeres, chromosome ends could fuse together and corrupt the cell’s genetic blueprint, possibly causing malfunction, cancer, or cell death. Because broken DNA is dangerous, a cell has the ability to sense and repair chromosome damage. Without telomeres, the ends of chromosomes would look like broken DNA, and the cell would try to fix something that wasn’t broken. That also would make them stop dividing and eventually die.

Why do telomeres get shorter each time a cell divides?

Before a cell can divide, it makes copies of its chromosomes so that both new cells will have identical genetic material. To be copied, a chromosome’s two DNA strands must unwind and separate. An enzyme (DNA polymerase) then reads the existing strands to build two new strands. It begins the process with the help of short pieces of RNA. When each new matching strand is complete, it is a bit shorter than the original strand because of the room needed at the end for this small piece of RNA. It is like someone who paints himself into a corner and cannot paint the corner.

Telomerase counteracts telomere shortening

Structure of the catalytic subunit of telomerase, TERT. From the Protein Data Bank (PDB entry 3DU5).

An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter, and the cells age.

Telomerase remains active in sperm and eggs, which are passed from one generation to the next. If reproductive cells did not have telomerase to maintain the length of their telomeres, any organism with such cells would soon go extinct.

Telomeres and cancer

As a cell begins to become cancerous, it divides more often, and its telomeres become very short. If its telomeres get too short, the cell may die. Often times, these cells escape death by making more telomerase enzyme, which prevents the telomeres from getting even shorter.

Many cancers have shortened telomeres, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.

Measuring telomerase may be a way to detect cancer. And if scientists can learn how to stop telomerase, they might be able to fight cancer by making cancer cells age and die. In one experiment, researchers blocked telomerase activity in human breast and prostate cancer cells growing in the laboratory, prompting the tumor cells to die. But there are risks. Blocking telomerase could impair fertility, wound healing, and the production of blood cells and immune system cells.

Telomeres and aging

Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.

While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of aging — like gray hair — or actually contribute to aging.

If telomerase makes cancer cells immortal, could it prevent normal cells from aging? Could we extend lifespan by preserving or restoring the length of telomeres with telomerase? If so, would that increase our risk of getting cancer?

Scientists are not yet sure. But they have been able to use telomerase in the lab to keep human cells dividing far beyond their normal limit, and the cells do not become cancerous.

If we used telomerase to “immortalize” human cells, we may be able to mass produce cells for transplantation, including insulin-producing cells to cure diabetes, muscle cells for treating muscular dystrophy, cartilage cells for certain kinds of arthritis, and skin cells for healing severe burns and wounds. An unlimited supply of normal human cells grown in the laboratory would also help efforts to test new drugs and gene therapies.

How big 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.

After 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.

Telomeres 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.

What are the prospects for human immortality?

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 sanitation measures, antibiotics, clean water, refrigeration, vaccines and other medical efforts to prevent children and babies from dying, improved diets, and better health care.

Some scientists predict average life expectancy will continue 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 oxidative stress damage could be repaired, “one estimate is people could live 1,000 years.”

Source: learn.genetics.utah.edu ~ Images: learn.genetics.utah.edu

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