Stayin alive

27 Jul

A hungry macrophlage eats an invader.  Sound effects added!  YouTube video credited to the School of Molecular and Cellular Biology University of Illinois at Urbana-Champaign.

Death typically happens to us just the once.  But our cells, which, in a way, are us, die all the time, literally billions of times every day.

Cellular death can be great for us. When we developed as embryos, our hands were “sculpted” by self-destructing cells that forged by their disappearance the space we see between our fingers.  Throughout our lives, patrolling cells in our bloodstream constantly look out for weak, feeble, infected and mutated cells that aren’t functioning, could contaminate other cells and would be best recycled.

But cells also die as the result of abuse, trauma, or disease, and in this context these mini-deaths at the cellular level begin to build up the potential for the big D at the body level.

Blobs in the arteries

In the case of heart disease—the leading cause of death in the United States—we get into trouble when the cells that clean up our bodily messes become overwhelmed.  White blood cells called macrophages (from the Greek for “big eaters”) troll about to consume debris, invaders, and worn out cells in our bodies, folding them into themselves and digesting them just like The Blob.  Macrophages will eat viruses, for example, that have been wrapped up by our antibodies that make them easier for the macrophages to grab; following the “dust to dust” principle that happens inside of us all of the time, the macrophages then digest the virus and antibodies and release their elemental parts.

But if the body is too chock full of cholesterol, the macrophages working to clear the arteries get overloaded and become foam cells that can no longer digest.  They are like boats sent out to clean pollution on a river.  If they become too mired in the debris, they become part of the logjam, and the water (or the blood in the vessel) is either diverted or dammed.

Depending on which of our arteries clog, we might have a stroke or a heart attack, kidney failure or, in the legs, peripheral artery occlusive disease (PAOD).

Rescue team failure

High blood pressure, smoking, and stress all cause damage, straining, nicking and cutting up our arteries.  When that happens, a coagulation team of molecules comes in like paramedics to lay down a patchwork of bandaging proteins that stop the bleeding.  But these scab wounds get left behind like orange cones at a construction site.  Inside the arteries, lipids (or fats) can get caught on those little scabs.  Smooth muscles underneath the arteries and macrophages all start coming in to try to fix the problem.   If there is just too much cholesterol plaque, the muscle cells enlarge and form a hard cover over the area that causes the artery to narrow, and the cells in the artery begin to calcify and die in this tar pit, becoming “necrotic tissues.”  In times of stress, some of the plaque will rupture, flow downstream, and get snagged further down the line, possibly blocking the artery. 

The death of cells causes blockages that can lead to the death of organs, which in turn can cause the whole body—us—to die.

Keeping our cells happy

So, if we’re not good to our cells, we’ve knocked a little bit of ourselves off. 

People tend to think of their bodies as cars: We feed them, see how fast they can go, and abuse the brakes and the tires as if we can get another one when she finally breaks down.  It probably makes more sense to think of our bodies as houses that need to be tended.  Like turtles, we have just the one shell to live in, so it helps to be mindful.

Protecting our cells means matching how we live externally to what we know about our body’s internal needs.  Eating fruits and vegetables instead of mystery chemicals, resting when we’re tired instead of eating, wearing sunscreen and reducing pollution can all keep our cells, and our selves, happy and well.

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