Normal Cell Death – The Body’s Suicide Program

Normal cell deaths occur in our bodies in large numbers all day, every day, often for the purpose of keeping our body in optimal working order. Many types of cells simply “wear out” and are subse­quently replaced by the replication of another cell nearby without any net loss to the body. But some cells die and are not replaced, like the neurons in our brains that die daily by the millions for an ever increasing net loss.

Cell deaths that are initiated by the body itself are the result of a “suicide program” that is written into the cell’s genetic code. Once activated, this program invokes a series of events that instruct the cell to kill itself. Known as a “apoptosis,” from the Greek for “fall­ing,” biology is loaded with examples of this phenomenon. There are cells in the immune system that will kill themselves after destroy­ing some foreign invader, others that kill themselves to keep an invading virus from replicating itself inside of them and spreading. There are also immune cells which can release chemicals that will initiate the suicide program in another cell’s DNA.

But why do cells have a built-in suicide mechanism anyhow? For starters, it protects the body from errant cells. It works like this: if the cell breaks away from the tissue where it belongs and ends up in some other part of the body where it doesn’t belong, it will automatically kill itself, thus putting a definitive end to its wander­ing ways.

Suicide may also keep cells within a tissue from dividing too much. For example, pancreas cells divide in a fetus until they take the form of a normal pancreas, at which point they stop via a suicide program that is then initiated—Hey, enough is enough, we’ve got the makings of a nice, functioning pancreas here and we still need room for a few other organs, so stop already!

Also, if a cell’s DNA becomes damaged and is in danger of becoming a cancer cell (a cell that keeps dividing indefinitely), sur­rounding cells sense the damage and very often will instruct it to kill itself.

But the suicide mechanism can work the other way around too, sending out antisuicide messages, and that is of special interest to those of us who are looking for ways to expand our Youthspan. Consider the embryonic nervous system. When it is developing in a fetus, many neurons will branch out and make contact with other neurons that are just about to kill themselves and send them a signal that says, in effect, “Don’t do it!”

In recent years, some antisuicide chemical messengers have been isolated by neuroscientists. Clearly one of the future steps for those of us who want to extend our Youthspan is to get these chemicals to tell certain critical, but suicide-prone cells to step back from the ledge.

The suicide and antisuicide mechanisms of neuron cells become particularly relevant when we start thinking about the various forms of dementia that can ruin the last 20 to 25 percent of our lives. Clearly, once a neuron in the brain is gone, that’s it—whole neuron files of memories and other functions are erased in the process and not another will appear to replace it. Therefore, our strategy must be to try to decrease the rate at which neurons die or accumulate damage over our lifetimes. And because some types of age-associated dementia seem to kick in when the suicide mechanism of neurons is turned on, we have to do what it takes to reduce their suicide rate.

But suicide is not the only natural cause of cell mortality. Even cells that have a healthy capacity for replicating themselves have a built-in death date, and that is where the Telomere Story comes in.