THE FOLLOWING is drawn from the second book in The Bipolar Expert Series, IN SEARCH OF OUR IDENTITY ...
In his classic book, The Selfish Gene, Oxford geneticist (and notorious militant atheist) Richard Dawkins asks us to think of the gene as an advanced version of a replicator, one that has developed a protective “vehicle,” a molecular survival machine to do its bidding. That survival machine may be as simple as a single-celled organism or as complex as a worm or a human being. Here, we are looking at evolution from the viewpoint of the gene, not the organism—the replicator, never the vehicle.
You may see yourself as the sum total of the 20,000 genes that comprise your genome. The gene, though, sees you as a sort of space ship, built to fend off a hostile environment and stay in one piece long enough to see its passenger(s) through to its manifest destiny of replication and reproduction.
Replication, though, doesn’t always go according to plan. A copying error may produce a slightly different version of the same gene. A faithful replication of the copying error means we now have two versions—alleles—of the same gene in circulation amongst the general population, each, technically, in competition.
Thankfully, a species can get along just fine with any number of versions of the same gene in circulation, with virtually no noticeable effect. Every once in a blue moon, though, something completely out of the ordinary takes place. To understand this, let’s go back in time to soon after the domestication of animals in the middle east around 10,000 years ago. There, in the blink of an eye, a lactose-intolerant human population became a lactose-tolerant one. Suddenly, a relative handful of individuals had a new food source which better equipped them for survival and reproduction.
One theory is these dairy farmers migrated into northern Europe with their herds and displaced an earlier generation of hunter-gatherers. There, milk’s high concentration of vitamin D conferred an added advantage, where winter sun is in short supply.
Thus, we see a spectacular example of a gene variant assuming dominance in a select population and that population taking over a continent. Much later, the history of these people would come to be written in terms of the inevitably of a mighty race—think of Thor with a milk mustache—traveling to distant lands and selflessly taking up the white man’s bounty, er burden.
But from a gene’s-eye view, we are simply talking about an overachieving random copying error, no more. It’s a matter of simple mechanics: Along a double strand of DNA inside the nucleus of the cell, we are able to identify a gene locus. In the case of the ability to digest milk, this would be LCT, whose “promoter region” initiates a chain of events that results in the formation of proteins from amino acids.
In this case, the protein takes the form of the enzyme lactase, which breaks down the lactose sugar found in milk. In the process, the lactase disintegrates back into amino acids, thus setting the scene for a new round of production.
In theory, this process can go on forever, but genes are “regulated”—that is, switched on or off— by neighboring stretches of DNA. In most human populations, lactase production is switched off for good during childhood. But, thanks to a chance variation, in certain populations the show goes on. Northern European humans are consuming milk and cheese.
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Moving the topic back to human behavior, it’s essential that we understand that the same gene-protein mechanics that regulate digestion—or, for that matter, the activity of ancient hydrogen-breathing microbes clustered around hydrothermal vents—also loom large in our behavior, but with this important proviso, namely: No gene or its variation will “cause” us to become, say, depressed. Rather, genes merely influence our chances of becoming depressed.
To best explain this, consider the neurotransmitter dopamine, which has been implicated in depression and mania, not to mention schizophrenia, ADHD, addictions, and so on, plus assorted behaviors such as novelty-seeking and experiencing pleasure. Our genome contains no shortage of DNA that regulate the many stages of dopamine’s life-cycle, from synthesis to neural messenger to metabolic breakdown.
This implies an infinity of things that can go wrong. On a cellular level, for instance, the neuron may fail to process the message the dopamine is supposed to be delivering. On a circuits and systems level, one region of the brain may be shouting while another is struggling to make itself heard.
Depending on circumstance and location, dopamine can be the hero or the goat. Too much, not enough. It may help make you smarter. Or it may set you up for an emotional crisis. There is actually a gene that appears to have a small influence on both. The gene is known as catechol-O-methyltransferase (COMT). Mechanically, COMT breaks down dopamine and other neurotransmitters. Those with a certain variation metabolize dopamine more slowly, which appears to enhance intelligence. The catch is the same variation may also result in greater emotional instability
A “good” gene variation or a “bad” gene variation, then? Answer, neither. The gene, itself, is not “consciously” coding for intelligence or emotional instability. It is simply turning out proteins. Maybe the owners of this particular gene variation thrive in their environment. Maybe their chances of attracting a mate are enhanced.
Or maybe not. Or maybe it doesn’t make all that much difference.
Thus, there are only accidents, accidents that in turn survive by more accidents, a series of accidents. Accidents of gene variations, accidents of environment. To illustrate this, let’s briefly consider attention deficit disorder, which is fairly common in the bipolar population. The condition involves a breakdown in dopamine signaling. Back in the days before schools and white collar work, the gene variations responsible would not have had the same crippling effect they do today. This is one of those Zen tree-falling-in-the-forest conundrums: Does a biological disorder exist if the social environment of the day fails to unmask it?
This is already evident in stress-related depression. The genetic vulnerability may exist, but if we are either lucky enough to lead a stress-free life or are particularly skilled in managing our stress, there won’t be all that many occasions where we will be putting that vulnerability to the test.
With ADD (or ADHD), because we tend to be talking about our kids, the issue gets particularly heated. This is not the place to get into all the arguments. But I will raise one small point. The other day, I was having a conversation with the mother of a nine-year-old daughter. She casually mentioned she had to have her at school for a 7:30 AM start.
What are we doing to our kids? I could only wonder. Of course their biology is going to protest. Introduce on top of that an otherwise insignificant genetic vulnerability and we’re playing with fire.
Everyone has their breaking point. I’n my case, I was an introvert doing an extravert’s job. Trying to adapt created its own set of stresses. Something had to give. Something did. Some unknown gene with a particular variation, perhaps. Maybe ten different genes. Maybe a hundred. Who knows? Bam! Accident meets accident. Suddenly, I could no longer rely on my brain to keep me sane.
Next thing, I was driving to my own Armageddon. I managed to pull back just in time, only to retreat into monkish isolation, shut off in my apartment, oblivious to the urbanized Eden just outside my door. If my future looked bleak to me at that point, imagine how my genes must have felt. Here I was, removed from the dating pool. Here they were, removed from the reproductive pool. If my mission on this earth—I had just one job!— was to serve them, then I had let them down completely. In my eyes, I was the most miserable being on earth. From their perspective, I was simply a failed vehicle with 20,000 disappointed replicators.
So it goes …
Dec 22, 2016
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