How we die

25 Jul

The shiny dots at the ends of these chromosomes are telomeres, the shortening "bomb fuses" that give cells expiration dates. Photo from the U.S. Department of Energy Human Genome Program

All roads lead to death, and we should all hope to take the scenic route.

                Some of us will pickle ourselves: We can smoke, drink, and burger our ways into Heaven.  Some of us will arrive instantaneously, let’s say, while texting.  But most of us will approach death along some kind of BINGO model.  One example:

                B: We’ve got atherosclerosis, or clogged arteries.

                I: We were born with something, like a propensity for high cholesterol.

                N: We have high blood sugar levels; G: We’re not exercising;  O: That one last cigar.


                As we age, everything sags, including the genome.

                We slow down.  Our nutritional needs plummet. We heal more slowly and become less adaptive.  We no longer build, we maintain. 

                Approaching death, signals go out throughout the cellular universes of our bodies that say, “We’re powering down.”  Just as we would handle the mess after a big party by breaking things down and filling up the recycling bin, everything in the body moves toward breaking down our cellular materials.  RNA starts to disappear, enzymes become protein shreds.  On most days, our chromosomes are like highways constantly traveled by polymerase, the enzyme that helps us make new chromosomes as cells divide.  But as the body dies, the cars get off the highway, and the scaffolding, or structural proteins that held up the roadway, begins to fall away.

At the species level, we can say that we die to make room for new generations.  Nature asks us to pass our genome along, to help our offspring to do the same, and then to step aside.  As humans we are lucky to be cast in nurturing roles as parents and grandparents.

Mayflies, which hatch, mate, lay eggs (if female) and die within hours, would have a lot to complain about, it they had the time.  As humans, we have the luxury of time to contemplate death, to study it, and sometimes, to find ways to postpone it.

            Our life expectancies have surged since 1900, mainly because of improvements in public health like vaccines and sanitation.  Americans can expect to live into their late 70s.

            A few not-unserious thinkers believe that humans will achieve immortality in the next 40 to 50 years.  Our young children or grandchildren, they say, might never die.   Futurists suggest two possible routes to eternal life: Via computers capable of downloading the full contents of the human mind, or through technologies that could indefinitely repair and rejuvenate the human body.

Eternal life for the body would mean overcoming the process of aging that takes place in our cells.

If disease or trauma don’t take us first, our cells eventually deteriorate, die, or lose the ability to divide.

The emerging field of epigenetics studies the networks of chemical switches that live inside our cells but outside of the gene sequence and affect how our genes behave.  The “epigenome,” which plays a major role in switching genes on and off, is a link between our genes and our environment.  It is affected by our diets, our habits, and life stories.

Like traffic cops, these mechanisms can make genes stop and go, can open up large tracts of chromosomes to be expressed or can shut them down.  As we age, they work in less synchrony, causing slow-downs throughout the body.  Certain genes are silenced.  After a lifetime of constant stress, body cells literally stop responding as if they were saying, “I’m already beat up: there’s nothing you can do to me.  Talk to the hand.”

Older people also have older cells.  Every time we scrape our knee or get a sunburn, stem cells need to divide to replace the injured tissues.  Over hundreds of divisions, epigenetic damage accumulates in our cells.

Another factor in aging is the telomere, the structures at the ends of chromosomes that make it possible for cells to divide—about 50 times, give or take.

Telomeres are like the plastic ends of shoelaces because they protect the strings of genetic data at the ends of our chromosomes.  But they’re also compared to bomb fuses, because they get shorter every time the cell divides.  A cell reaches its “Hayflick limit” when the telomeres become too short for the cell to divide.  (For a great intro to telomeres, see this web page and podcast from the University of Utah’s Genetic Science Learning Center.)

Telomerase, an enzyme that is active in a few cells, including eggs and sperm and embryonic stem cells, allows cells to replace the “shoe lace” ends on the chromosomes and to go on dividing beyond their normal limit.  The prospect of creating “immortal cells” is exciting, but telomerase is not a simple antidote to aging and death because this same process of extending the lifespan of cells is also a step toward enabling cancerous growth.  Short telomeres are linked to aging, but not necessarily the cause; they could be just a symptom, or just another letter in the BINGO game.

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