What is aging? Your body is composed of millions of cells that keep you alive and active. Some cells can replace themselves, but many cannot. Over time, those cells deteriorate to the point where they cause a tissue or organ to fail. Sometimes an organ can be repaired or replaced, but when enough failures occur (or a vital organ fails), we die.
A good analogy is your automobile. When you drive it new from the dealer, all systems work well. If you do preventive maintenance, the car will run for a long time. But as time goes by, components wear out and fail. You take the car to a garage and replace defective parts. As the car gets older, more components wear out. This is aging and is true with your body. As we age, we need to replace or repair worn-out organs and tissues.
What causes aging? Currently, there are three theories that try to explain the cause of aging.
1. Our cells and tissues simply wear out over time. Cells are made of several thousand different kinds of proteins. (We are walking blobs of protein.) They are the structure of cells and the many different machines inside cells that keep us alive. Proteins are long chains of amino acids folded in unique ways. The trouble is that wear causes the chains of amino acids to unfold, and unfolded proteins stop working. This causes cells to deteriorate. Some scientists proposed that oxidizers wreck proteins, much as they rust steel. Oxidation may contribute to cell deterioration, but oxidizers are not the single cause of aging. Research has found that antioxidants do not stop us from aging and do not extend life. If the cells-wearing-out theory is correct, the way to stop aging is by repairing or replacing worn-out cells, tissues, or organs, just as we would do with our car.
2. Telomeres control lifespan. Telomeres are strings of DNA at the ends of chromosomes. Each time a cell divides, it shortens the telomeres. As they shorten, the cell exhibits the deterioration of aging. An enzyme, telomerase, can restore telomeres. But when a cell matures, telomerase switches off. If we can reactivate telomerase, an aging cell can become a young cell, but if telomerase is unchecked, it makes cells continue to divide to form a cancer. If telomerase is to prevent aging, we must develop a drug that allows telomerase to stop aging, but not cause cancer.
3. Genes control aging and lifespan. Some families pass on the trait of long life to generation after generation. In laboratory animals, mutation of certain genes extends life span two to five times. These genes limit life, so blocking their action extends life. Similar genes occur in humans. These genes probably block the action of enzymes that repair damaged proteins or DNA. If we develop a drug that blocks life-limiting genes to give comparable extension of human life, it could give healthy people a life span of 500 years or more. Researchers are working hard on these genes.
Which theory is correct? There are scientists who lean toward each and are doing research on each. If research on life-shortening or life-extending genes finds drugs that controls these genes or their products, then we may have the means to prevent aging. The same may be true if research leads to drugs that control telomerase. In the meantime, we may be able to slow aging by preventive maintenance and repair with drugs, organ replacement, and stem cells.
The question is not whether we will conquer aging. The question is when. In Hello Methuselah, I projected, from the rate of research progress, that we will begin to control aging by 2030 and control it by 2050. It is a bright future.
Recent Discoveries.
1. Petrascheck, et al., An Antidepressant that Extends Lifespan in Adult Caenorhabditis elegans. (Nature, 450, November 22, 2007). To find drugs that will extend lifespan, 88,000 chemicals were tested for ability to extend the life of adult Caenorhabditis elegans. One drug, the antidepressant mianserin, extended lifespan by 30%, seemingly by mimicing the effect of calorie restriction. .
2. Pinkston and coworkers, Mutations that Increase the Life Span of C. elegans Inhibit Tumor Growth. (Science, 313, August 18, 2006). It has been thought that actions that suppress aging also increase cancer formation. Experiments show instead that mutations which extend life-span also inhibit cancer formation.
3. Bjezakovic and coworkers, Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention. (Journal of the American Medical Association, 297, February 28, 2007). In a review of 68 trials involving 232,606 people, researchers found that beta-carotene, vitamin A, and vitamin E did not increase longevity. In fact, they increased mortality. Vitamin C and selenium had no significant effect.
4. Autier, P. and S. Gandini, Vitamin D Supplementation and Total Mortality. (Archives of Internal Medicine, 167, September 10, 2007). Intake of vitamin D supplements seems to correlate with decreased mortality.
5. Cherkas, L.F., et al., The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length. (Archives of Internal Medicine, 168, January 28, 2008). Physical activity slowed the shortening of telomeres that is associated with aging, and thus may slow the aging process.