Several aging mechanisms are known, and anti-aging therapies aim to correct one or more of these:
- Dr. Leonard Hayflick discovered that mammalian cells divide only a fixed number of times. This "Hayflick limit" was later proven to be caused by telomeres on the ends of chromosomes that shorten with each cell-division. When the telomeres are gone, the DNA can no longer be copied, and cell division ceases. In 2001, experimenters at Geron Corp. lengthened the telomeres of senescent mammalian cells by introducing telomerase to them. They then became youthful cells. Sex and some stem cells regenerate the telomeres by two mechanisms: Telomerase, and ALT (alternative lengthening of telomeres). At least one form of progeria (atypical accelerated aging) is caused by premature telomeric shortening. In 2001, research showed that naturally occurring stem cells must sometimes extend their telomeres, because some stem cells in middle-aged humans had anomalously long telomeres.
- Experimenters discovered that mice whose pituitary glands were removed lived half again as long as unmodified mice, though with terrible side-effects. Therefore, mammals are believed to have a hormonal system that triggers some age-related disease.
- In 2002, genetic modification of a small annelid worm (C. elegans) increased its lifespan sixfold. Related experiments have increased maximum life-span in mice and fruitflies. These experiments prove that there is a genetically-coded death clock that triggers some part of aging. This may be related to the hormonal death clock.
- A number of research programs have proven that mutations in body cells occur and accumulate as an organism ages, and degrade its function. In 1999, researchers discovered that naturally occurring stem cells recolonize organ systems, countering this effect by reintroducing cells from a reduced number of cellular lineages.
- A number of clinicians noted that the cumulative damage in diabetic patients strongly resembled accelerated aging. This was generalized into a theory that some aging is caused when sugar chemically combines with proteins and other bodily chemicals. It is known that feeding adolescent mice a fully-nutritive diet with minimal calories can extend their maximum life-spans by half. It is also known that feeding mice small amounts of chromium picolinate can extend their maximum life span about 15%. Chromium is an integral part of active insulin, and insulin is cleaved, to excrete chromium in normal metabolism. Most adult nonvegetarians have large amounts of inactive insulin, which may indicate a chronic deficiency of dietary chromium. Veterinarians routinely treat middle-aged animals for diabetes with chromium supplementation.
- Studies of patients with Alzheimer's disease patients and age-spotting discovered that the body builds deposits of waste within and without cells. The deposits inside cells are called "lipofuscin" (latin for "fat dirt"). These deposits may decrease metabolic efficiencies, causing some age-related symptoms. Mammalian cells have enzymes to cleave and digest proteins. The most common such clean-up enzyme is triggered by a three-element chain of Ubiquinone (CoQ10) attached to the elderly protein.
- Dr. Dennis Harman theorized that some aging damage might be caused by oxidative damage to the body. Experiments discovered that the body has substantial amounts of enzymes and chemicals to reverse oxidative changes. Studies also showed that longer-lived animals have larger amounts, per weight of animal of these mechanisms, in a linear relation to life-span. The experiments also found an internal mechanism, respiration in mitochondria, that creates free radicals that would cause oxidative damage. Feeding of antioxidants to mice increased average life-spans, but not maximum life spans. It is now believed that oxidative damage depletes self-repair mechanisms, whose limits are controlled by other systems.
- Caloric restriction has consistently extended the maximum life-spans of laboratory animals. It works on every animal in which tests have been completed, from rotifers up to guinea pigs, and preliminary results on Rhesus monkeys are promising. It was first popularized by Dr. Roy Walford. Unfortunately it is acutely uncomfortable. Also, the program must be started in young adulthood for maximum benefit. Some studies with mild caloric restriction have had some benefit when started on middle-aged mice, but the extreme programs started with young mice actually reduce maximum life-spans of middle-aged mice. Caloric restriction can be implemented either as reduced regular feeding, or as days of fasting alternating with days of free-feeding.
- Research on drugs to mimic caloric restriction continues. In 2003, the Life Extension Foundationfunded gene-chip research comparing gene expression in calorically-restricted mice with the gene expressions of mice on various prescription drugs, including especially diabetic drugs. The researchers found that the diabetic drug Metformin (trade-marked Glucophage) had identical gene expression in mice, within the limits of measurement.
- Stem cell therapy would be used to replace damaged or diseased cells in living tissue.
- Gene therapy to repair damaged or diseased cells (including cancer). This would include extension of teleomeres to reduce cellular aging and induced failures of telomerase to prevent growth of cancers.
- Breaker medication to remove glycosylated (sugar-damaged) proteins and to restore elasticity to the organs, especially the heart. The most famous is l-acetyl carnitine, an amino salt available in health-food stores in the U.S.
- Supplementation of chromium to increase insulin efficiencies and reduce blood sugar loads.
- Antioxidants to reduce oxidative damage to the body. This does not extend maximum life span, but does increase average life-spans in a population of mice, indicating that it does reduce metabolic damage. Popular ones include vitamins E, and C. Certain natural antioxidant enzymes, superoxide dismutase is the most common, require adjuvant minerals on their active sites. The most common form of superoxide dismutase requires an atom of selenium. Another common dismutase requires an atom of copper, another zinc.
- A widely-known therapy against lipofuscin (waste build-up in the cell) is large doses of an enzymic cofactor called ubiquinone, or CoQ10. CoQ10 forms chains attached to proteins. A chain of three CoQ10 molecules marks a protein as "old" and allows cellular digestive enzymes to attach to it and cleave it. Heavy chronic doses of CoQ10 can gradually reduce senile confusion, lower blood pressure, and cause age-spots to fade. CoQ10 is available as a supplement in most U.S. health food stores.
- Hormone therapies partially reverse some of the effects of aging. Growth hormone supplementation reverses many of the hormonal effects of aging, including sexual hormones, and losses of muscle and immune function. In mice, it reduces maximum life-span slightly, while slightly increasing average life-span. Hormone therapies with sex hormones (i.e. estrogen or testosterone) or their precursors (DHEA) are more controversial. Although sexual functions increase, side effects to other body systems are substantial.
- Persons interested in life extension are often interested in cryonics, as a risky but scientifically-plausible alternative to certain death from age-related damage. However cryopreservation can cost from thirty thousand (Cryonics Institute) to a hundred and twenty thousand dollars (Alcor Life Extension Foundation). It is usually funded by life insurance, but the amount of required life insurance may be impractical to purchase for the elderly, or unhealthy people in late middle age.
- The Alcor Life Extension Foundation
- The Cryonics Institute
- The Immortality Institute
- Life Extension Foundation
- Strategies for Engineered Negligible Senescence (SENS)
- Mechanisms of Aging
- Why Life Extension or Why Live at All?
- The NanoAging Institute