posted on Dec, 6 2007 @ 10:46 PM
Multiple reasons for the phenomenon we call ageing...happens to be part of my field.
1. We are designed to reproduce and raise young; after we hit 30, we are no longer in the evolutionary game so to speak, so evolution has given up on
us at that point and we are stuck with what we have at that point; if we reproduced until we were 100, we would stay "young" till we were 100, like
giant turtles, trees, some fish. Why did nature pick about 30? It's because of our environment for most of human history which caused our lives to
be brutally hard and very short. Because we have bodies that were designed/evolved for stone age life when odds were we wouldn't survive beyond that
due to infection, trauma, murder, disease, etc. It's an odds game. Mice live about 2 years because odds are they will be eaten before then; we live
about 30 years without medical assistance on average because odds were that we would get killed or eaten by that age in the wild.
2. Chemically, we age because of several factors. The most superficial level is that we no longer produce proteins in the correct amount and with
adequate function and we no longer produce hormones that tell the cells what to do in appropriate amounts. Menopause is the most obvious example, but
all the hormones except cortisol drop with time; eventually cells just stop working due to no instructions from the "home office", ie the
hypothalamus and pituitary. Enzymes are misformed or formed in inadequate quantities, so food is not absorbed or metabolized and the cells starve.
3. The next level is at that of the mitochondria. The DNA of the mitochondria, the structure in the cell that produces ATP for energy, has no repair
mechanism. When it gets damaged by oxygen free radicals, the damage persists. Eventually the mitochondria stop working efficiently because the DNA
instructions for vital proteins are screwed up. Some die off, but others reproduce; if they have damaged DNA then all the mitochondria in the cell
will eventually be defective=energy shortage=cells malfunction or die=ageing.
4. At the cellular DNA level, there are 2 main problems. The telomeres, the terminal DNA segments at the end of the chromosomes get shorter with
each cell division. When they get to a certain length, the tumor suppressor genes p53 and others are activated and the cell terminates or the cell
just goes dormant, unless it can mutate into a cancer cell and survive. This is the so-called Hayflick limit. In humans, cells replicate about 50
times before this happens. Stem cells can extend their telomeres and so they stay young. Interestingly, even at old age, only about 15% of an
old-person's cells have reached this point, so there is still a lot of potential life in them. We think that the senescent cells secrete factors
that cause their neighboring cells to malfunction.
5. Beyond that is the problem of glycation where glucose molecules become chemically attached to DNA and proteins and impair their function. Thus,
diabetics have premature ageing. Proteins also cross-link and stop being flexible=wrinkles.
6. Inflammation causes degeneration of all the body tissues and increased production of free radicals, accelerating aging.
That was a brief summary. The good news is that each of these problems is preventable and treatable and treatment has actually been proven to work in
animals; trials in humans are underway right now to lengthen telomeres and potentially create immortality if the other issues are addressed. The
first group underwent treatment this year, results show increased telomere length in peripheral leukocytes. Clinically they seemed younger, but it is
really too soon to tell. The thorniest problem is repairing damaged mitochondria; we can enhance their function with chemicals, but no one knows how
to replace them in a living cell. That is the key.