A darker shade of gray
I still remember the first time I heard these lyrics over the car radio: “Ooh, what a lucky man he was.” I got goose bumps. I was amazed as the song ended with one of the strangest keyboard sound clusters I’d then encountered. I didn’t normally listen to rock in those days—still don’t (I prefer Stravinsky to the Stones), but I wanted to know more about this group. It was a trio, sporting a name more like a law firm than one of the great prog-rock groups of the ’70s: Emerson, Lake & Palmer. When I discovered they also did electronic covers of classical pieces, it was love at first toccata. I was especially enamored of the virtuosity of the group’s legendary keyboardist, Keith Emerson. Thus it was with sadness that I read about Emerson’s suicide, in 2016, at age seventy-one. Though he kept the dogs of depression at bay for years, his resistance ended when he developed career-threatening nerve damage to his fingers. Gun in hand, he became not such a lucky man after all.
Depression and suicide go hand in hand, as Emerson’s life illustrates. Depression and old age go hand in hand, too, which his life also illustrates, and this represents the deepest shade in the dark side of our chapter on happiness. It also seems to contradict virtually everything I’ve been discussing so far. I obviously have some explaining to do. And with help from two quotes in the research literature, I intend to do just that.
First, we need a quick definition of depression. That’s important because people often confuse depression with normal sadness. In fact, seniors in the grips of depression often don’t feel particularly sad. Instead, they become increasingly unfocused and demonstrably more irritable and restless, and they experience a steady erosion in things they used to find pleasurable. We also need to take into account the fact that triggers for depression—health failures, deaths of loved ones, unremitting pain—are routine events for the elderly.
Older literature about senior depression, such as our first quote (from the surgeon general of the United States, circa 1999), says things like: “Depression is not a normal part of aging . . . serious depression is not ‘normal’ and should be treated.” True? Though the appeal for treatment is spot-on, later research showed the rest of that quote is true only if you don’t look too closely. If you do look closely, you run right into our second quote (from researcher Ke-Xiang Zhao, at Chongqing Medical University in China), which takes issue with the idea that depression isn’t typical: “Older age appears to be an important risk factor for depression in the general elderly population (aged below 80 years).”
Reconciling these seemingly different perspectives, it turns out, depends on how often you had to visit the hospital. For moderately healthy seniors, depression isn’t typical. For seniors whose health is impaired, it’s a different story. (And it’s a good thing that researchers made the distinction, because if they lumped everyone together, they could be fooled into thinking they’re looking at “natural erosion” rather than “unnatural disease progression.”)
Here’s what we know now: the more health challenges seniors encounter, the greater their depression risk becomes. The type of disability is the major contributor, with chronic disease taking pole position. One of the biggest contributors to depression is hearing loss. Another biggie is vision loss. Others are the various cancers, chronic lung diseases, strokes, and cardiac diseases. Unknown are the effects of diabetes and hypertension.
If seniors live in community settings, depression chimes in at a modest 8 percent to 15 percent. Hospitalize them because of some physical ailment, or simply put seniors into assisted living, and the prevalence soars to 40 percent. That’s a big deal. Depression is now projected to be the leading cause of disease burden in the elderly by 2020. The bottom line is that happiness increases in older populations as long as seniors remain healthy. But since health naturally ebbs in aging populations, the rate of depression rises.
Is there something we can do? Though the answer is yes, we must revisit some brain biology to understand our options, examining one of the happiest biochemicals on earth. Would that Keith Emerson could have become better acquainted with it.
Dopamine’s decline
“That’s the problem,” my dad chuckled one cold winter morning in 1966, holding up a small, jewel-like bauble for me to inspect. It looked like the threaded end of a decapitated Christmas light. “If we replace the old guy with this one, the kitchen’s gonna work good as new.”
Earlier that morning, my ten-year-old self had marched into his bedroom, horribly alarmed that I had broken the entire kitchen. I had plugged in a portable space heater near the fridge, then heard a loud pop. The kitchen immediately stopped working. No lights, no refrigerator, no stove, no electric can opener.
“All you did was blow a fuse, Son,” my dad said, fingering his glittering electrical ornament, a spare (now vintage) fifteen-amp household fuse. I was amazed. How could such extensive culinary destruction—from refrigerators to ovens—result from something so small, so singular? I got my first lesson in how electrical circuits worked in houses. Dad unscrewed the old fuse and put in the new one; sure enough, the kitchen roared back to life.
This electrical nostalgia illustrates something useful about brain wiring and its activating circuitry. I’ve mentioned many behavioral changes in this chapter: decision making, award seeking, risk taking, selective memory, depression. These behaviors might seem as functionally disconnected as a can opener from a freezer. But they aren’t disconnected at all. Scientists believe the biological basis for most of these changes comes from the failure—just like in that kitchen—of a single circuit.
This circuit isn’t made of wires responding to electricity, of course; it’s made of neurons responding to a neurotransmitter. The neurotransmitter is a famous molecule I’ll bet you’ve heard of before: dopamine. The circuits over which dopamine exerts its powers are called dopaminergic pathways. The brain has about eight of these pleasure-coaxing pathways.
One of the first impressions you’d get if you ever bumped into a molecule of dopamine is how ridiculously small it is. It’s synthesized by redecorating an amino acid called tyrosine. Remember amino acids from high school biology? They’re the natural building blocks of proteins. To make a protein, long strings of amino acids—sometimes hundreds—are strung together like cars in a train. Dopamine is the size of just one of those train cars.
You may also be familiar with tyrosine because of your diet. Most of you eat it every day. Egg whites have a lot of tyrosine. So do soybeans. And seaweed. Don’t be fooled by its size or pedestrian origins, however. Dopamine packs a serious wallop. Make too little of it and you might get Parkinson’s disease. Make too much of it and you might get schizophrenia. When you synthesize just the right amounts, dopamine mediates your ability to reward yourself with pleasure, your ability to hold a pen without shaking, and your ability to make decisions. Every one of the behaviors mentioned in this chapter at some level involves dopamine. Impressive skill set for a clump of seaweed.
How does this polymath of a molecule do it? Dopamine mediates its activities by binding to a family of receptors built for it. These receptors are found only on certain neurons in the brain. Cells lucky enough to sport the receptors are activated to perform certain functions when dopamine binds to them. Think of it as the ignition system inside your standard Honda. Insert the key into the lock, and the car springs to life. Insert the dopamine into its neuron-bound receptor, and the neuron springs to life. Put many of those neurons in a row, and you have an activatable circuit. Put eight or so of those circuits together, stuff them deep into the center of the brain, and you have the dopaminergic system.
Given the brain’s