Aging is not a disease

Aging is a concept generated by human experience to describe the decay that we expect as we journey through time.

Time is the central organizing principle of our lives from cradle to grave. Some philosophers believe in time; others believe it is created by man to measure. But is it really a fundamental property of the universe like subatomic particles and the energies of electromagnetism, nuclear forces, and yet undiscovered fields?

You're not the man you used to be

The preceding paragraph may sound like mumbo-jumbo but ask yourself whether a undriven '67 Mustang is still a '67 Mustang if you've only kept it in a dust-proof vault. Or what if you've replaced all the parts with modern ones? Like cars and progeric kids, we age not because of the passage of "time" but as a function of our mileage, maintenance, and accident history.

Speaking of replacement parts, did you know many scientists believe that NONE of cells comprising your body were present ten years ago. You are comprised entirely of new cells generated from stem cells in your body.

Good news for ex-party animals!

Received wisdom tells us that you can't make new brain cells. Actually, your hippocampus, a site of memory generation, makes about 10,000 new neurons a day using neural stem cells. When you sleep, your memories are pruned and organized for eventual storage in the cerebral cortex. How awesome is that?

And by the way, fossil fuels are not made from dinosaurs.

Science marches on but received wisdom lags.

That is why we should oppose the delusion that fighting aging is impossible simply because the universe would never be that kind to us. The "too good to be true" school of thought represents true magical thinking, not the scientifically-verifiable findings of telomere biology.

Current Theories of aging

Intracellular junk

Cells must clear waste products but when they grow old (or senescent) you can observe small bags of junk inside them and large bags of junk outside them.

But is the junk the cause or the result of dysfunction? Unless you've figured out the "chicken or the egg" quandary, the jury will be out on this theory for a while.

Mitochondrial Manchurian Candidates:

Each cell hosts hundreds of mitochondria, the symbiotic critters that generate the energy in the form of ATP. In our old age, our mitochondria sabotage our cells in a variety of ways. They become like Homer Simpson at the nuclear power plant, pouring out reactive oxidative species (ROS) that are a danger to themselves and the host. Although anti-oxidants are widely touted by anti-aging salesmen, taking anti-oxidants is like trying to put out a kitchen fire by spraying the outside of the house. The problem is indoors, or in the cellular compartment.

The ROS theory of aging may reflect a "red herring" insofar as the host cell's own genetic errors and resultant protein and RNA dysfunction may elicit the destructive interaction with the previously friendly mitochondria.

Interestingly, the mitochondria may be involved in telomerase regulation in, as yet, unknown ways.

Telomere shortening in stem cells

If this is the first you're hearing about telomeres, you're in good company; most physicians have never heard of them either. But go to the US National LIbrary of medicine, PubMed, and type in "telomere" - you'll retrieve over 10,000 articles in the scientific literature.

In the laboratory, telomerase activation by TA-65 has been shown to lengthen telomeres and support cellular immune function. After a year of ingestion, Dr. Park has grown younger in appearance and subjective well-being. His continuous review of the scientific literature has led him to propose this simple and integrated theory of aging:

Axiom 1: Because of the mechanics of copying DNA, telomeres always grow shorter with cell divisions.

Axiom 2: Stem cells and Cancer cells (possible mutant stem cells) are capable of self-immortalizing by lengthening their telomeres with telomerase.

Corollary 2.1: telomere length in stem cells is dynamic and lengthens or shortens as a a function of telomerase activation, replicative burden, and environmental effects.

Axiom 3: Differentiated, or non-stem cells cannot be younger (telomere length) or healthier (genetic integrity) than their most recent stem cell progenitor.

Corollary 3.1: Since T-cells of the cellular immune system are all stem-like in nature, a senescence of T-cells results in worsening immune function reflected in higher rates of infection and cancer

Axiom 4: For non-stem cells, which don't produce an active form of telomerase, the Hayflick Limit is the cause of apoptosis ("programmed" cell death) and teleologically serves to protect us from rogue cell lines that have acquired dangerous changes from DNA transcription errors, erroneous splicing, and oxidative or ionizing stresses.

HYPOTHESIS: Aging is caused by the shortening of telomeres in stem cells. If the stem cells' telomeres can be protected by telomerase activation, then the effects of aging may be slowed and possibly reversed