armpits

Genetic determinism: why we never learn—and why it matters

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Here it is, 2014, and we have “Is the will to work out genetically determined?,” by Bruce Grierson in Pacific Standard (“The Science of Society”).

Spoiler: No.

The story’s protagonist is a skinny, twitchy mouse named Dean who lives in a cage in a mouse colony at UC Riverside. Dean runs on his exercise wheel incessantly—up to 31 km per night. He is the product of a breeding experiment by the biologist Ted Garland, who selected mice for the tendency to run on a wheel for 70 generations. Garland speculates that Dean is physically addicted to running—that he gets a dopamine surge that he just can’t get enough of.

Running in place

Addiction theory long ago embraced the idea that behaviors such as exercise, eating, or gambling may have similar effects on the brain as dependence-forming drugs such as heroin or cocaine. I have no beef with that, beyond irritation at the tenuous link between a running captive mouse to a human junkie. What’s troubling here is the genetic determinism. My argument is about language, but it’s more than a linguistic quibble; there are significant social implications to the ways we talk and write about science. Science has the most cultural authority of any enterprise today—certainly more than the humanities or arts!. How we talk about it shapes society. Reducing a complex behavior to a single gene gives us blinders: it tends to turn social problems into molecular ones. As I’ve said before, molecular problems tend to have molecular solutions. The focus on genes and brain “wiring” tends to suggest pharmaceutical therapies.

To illustrate, Grierson writes,

File this question under “Where there’s a cause, there’s a cure.” If scientists crack the genetic code for intrinsic motivation to exercise, then its biochemical signature can, in theory, be synthesized. Why not a pill that would make us want to work out?

I have bigger genes to fry than to quibble over the misuse of “cracking the genetic code,” although it may be indicative of a naiveté about genetics that allows Grierson to swallow Garland’s suggestion about an exercise pill. Grierson continues, quoting Garland,

“One always hates to recommend yet another medication for a substantial fraction of the population,” says Garland, “but Jesus, look at how many people are already on antidepressants. Who’s to say it wouldn’t be a good thing?”

I am. First, Jesus, look at how many people are already on anti-depressants! The fact that we already over-prescribe anti-depressants, anxiolytics, ADHD drugs, statins, steroids, and antibiotics does not constitute an argument for over-prescribing yet another drug. “Bartender, another drink!” “Sir, haven’t you already had too much?” “Y’know, yer right—better make it two.”

Then, what if it doesn’t work as intended? Anatomizing our constitution into “traits” such as the desire to work out is bound to have other effects. Let’s assume Dean is just like a human as far as the presumptive workout gene is concerned. Dean is skinny and twitchy and wants to do nothing but run. Is it because he “wants to exercise” or is it because he is a neurotic mess and he takes out his anxiety on his wheel? Lots of mice in little cages run incessantly—Dean just does it more than most. His impulse to run is connected to myriad variables, genes, brain nuclei, and the reported results say nothing about mechanisms. We now know that the physiological environment influences the genes as much as the genes influence physiological environment. The reductionist logic of genetic determinism, though, promotes thinking in terms of a unidirectional flow of causation, from the “lowest” levels to the “highest.” The more we learn about gene action, the less valid that seems to become as an a priori assumption. The antiquated “master molecule” idea still permeates both science and science writing.

Further, when you try to dissect temperament into discrete behaviors this way, and design drugs that target those behaviors, side effects are sure to be massive. Jesus, look at all those anti-depressants, which decrease libido. Would this workout pill make us neurotic, anxious, jittery? Would we become depressed if we became injured or otherwise missed our workouts? Would it make us want to work out or would it make us want to take up smoking or snort heroin? In the logic of modern pharmacy, the obvious answer to side effects is…more drugs: anti-depressants, anxiolytics, anti-psychotics, etc. A workout pill, then, would mainly benefit the pharmaceutical industry. When a scientist makes a leap from a running mouse to a workout pill, he is floating a business plan, not a healthcare regimen.

And finally, what if it does work as intended? It would be a detriment to society, because, having a pill, it would remove yet another dimension of a healthy lifestyle from the realm of self-discipline, autonomy, and social well-being. It becomes another argument against rebuilding walkable neighborhoods and promoting public transportation and commuting by bicycle. A quarter-mile stroll to an exercise addict would be like a quarter-pill of codeine for a heroin junkie—unsatisfying. Not only is this putative workout pill a long, long stretch and rife with pitfalls, it is not even something worth aspiring to.

And that’s just one article. Scientific American recently ran a piece about how people who lack the “gene for underarm odor” (ABCC11) still buy deodorant (couldn’t possibly have anything to do with culture, could it?). Then there was their jaw-dropping “Jewish gene for intelligence,” which Sci Am had already taken down by the time it appeared in my Google Alert. I’d love to have heard the chewing out someone received for that bone-headed headline. Why do these articles keep appearing?

The best science writers understand and even write about how to avoid determinist language. In 2010, Ed Yong wrote an excellent analysis of how, in the 1990s, the monoamine oxidase A (MAOA) gene became mis- and oversold as “the warrior gene.” What’s wrong with a little harmless sensationalism? Plenty, says Yong. First, catchy names like “warrior gene” are bound to be misleading. They are ways of grabbing the audience, not describing the science, so they oversimplify and distort in a lazy effort to connect with a scientifically unsophisticated audience. Second, there is no such thing as a “gene for” anything interesting. Nature and nurture are inextricable. Third, slangy, catchy phrases like “warrior gene” reinforce stereotypes. The warrior gene was quickly linked to the Maori population of New Zealand. Made sense: “everyone knows” the Maoris are “war-like.” Problem was, the preliminary data didn’t hold up. In The Unnatural Nature of Science, the developmental biologist Lewis Wolpert observed that the essence of science is its ability to show how misleading “common sense” can be. Yet that is an ideal; scientists can be just as pedestrian and banal as the rest of us. Finally, Yong points out that genes do not dictate behavior. They are not mechanical switches that turn complex traits on and off. As sophisticated as modern genomics is, too many of us haven’t moved beyond the simplistic Mendelism that enabled the distinguished psychiatrist Henry H. Goddard to postulate—based on reams of data collected over many years —a single recessive gene for “feeblemindedness.” The best method in the world can’t overcome deeply entrenched preconception. As another fine science writer, David Dobbs, pithily put it in 2010, “Enough with the ‘slut gene’ already…genes ain’t traits.”

As knowledge wends from the lab bench to the public eyeball, genetic determinism seeps in at every stage. In my experience, most scientists working today have at least a reasonably sophisticated understanding of the relationship between genes and behavior. But all too often, sensationalism and increasingly greed induce them to oversell their work, boiling complex behaviors down to single genes and waving their arms about potential therapies. Then, public relations people at universities and research labs are in the business of promoting science, so when writing press releases they strive for hooks that will catch the notice of journalists. The two best hooks in biomedicine, of course, are health and wealth. The journalists, in turn, seek the largest viewership they can, which leads the less scrupulous or less talented to reach for cheap and easy metaphors. And even though many deterministic headlines cap articles that do portray the complexity of gene action, the lay reader is going to take away the message, “It’s all in my genes.”

Genetic determinism, then, is not monocausal. It has many sources, including sensationalism, ambition, poor practice, and the eternal wish for simple solutions to complex problems. Science and journalism are united by a drive toward making the complex simple. That impulse is what makes skillful practioners in either field so impressive. But in clumsier hands, the simple becomes simplistic, and I would argue that this risk is multiplied in journalism about science. Science writing is the delicate art of simplifying the complexity of efforts to simplify nature. This is where the tools of history become complementary to those of science and science journalism. Scientists and science writers strive to take the complex and make it simple. Historians take the deceptively simple and make it complicated. If science and science journalism make maps of the territory, historians are there to move back to the territory, in all its richness—to set the map back in its context.

Studying genetics and popularization over the last century or so has led me to the surprising conclusion that genetic oversell is independent of genetic knowledge. We see the same sorts of articles in 2014 as we saw in 1914. Neither gene mapping nor cloning nor high-throughput sequencing; neither cytogenetics nor pleiotropy nor DNA modification; neither the eugenics movement nor the XYY controversy nor the debacles of early gene therapy—in short, neither methods, nor concepts, nor social lessons—seem to make much of a dent in our preference for simplistic explanations and easy solutions.

Maybe we’re just wired for it.

News of genes for: the latest examples—and further reflections on why we persist in believing in them

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There is a basic contradiction in the lay response to genome news. Somehow, the more we learn about how complex and nuanced gene action is, the more we seem drawn to “gene-for” explanations. Collectively, we know that genes do not directly determine or control traits, let alone behaviors. And we know that single genes do not produce complex traits, except (maybe) in a few extreme and rare circumstances. There are no genes for; and yet we keep talking about them—possibly more than ever. Why is that?

Individual cases, drawn from current events, both demonstrate my premise and give us some leverage for prying apart the halves of this paradox.

So let’s roll up our sleeves and get started.

 

I stink, therefore I scam

One of the less appetizing findings of genetics is that if you can’t roll your earwax up into a nice, satisfying ball, your gym buddies in all likelihood choose lockers disconcertingly far from yours. The gene ABCC11 codes for a protein that is involved in the consistency of earwax—and that is apparently quite nutritious to the bacteria that produce body odor. There is, in short, a “key gene” that is “basically the single determinant of whether you produce underarm odor or not,” said Ian Day, a co-author of a new study on the behavior genetics of raunchy pits.

All this has been known for some time. A new paper, by Day and colleagues and published in the Journal of Investigative Dermatology, found that many people who lack “the underarm odor gene” nevertheless still wear deodorant.

One the one hand, this shows that genetics often makes very little difference in our lives. I haven’t confirmed the result with my own nose, but accepting for the moment that ABCC11 does in fact code a protein largely responsible for body odor, apparently few people are paying much attention to it. More important than whether we are actually olfactorily offensive, seemingly, is the marketing ploy that presents human beings as innately stinky creatures, who, in order to be socially successful, need to neutralize our natural stench with perfumes and deodorants. We deodorize independently of the presence of body odor.

On the other hand, then, although we are not slaves to our genes, this study suggests that we are slaves to our culture. Cultural norms and values often shape our behavior more than biological “reality.”

Nor surprisingly, the allele frequency for dry earwax/odorless axilla (the anatomical term for armpit; the middle-schoolers in your life will be thrilled to know this term) varies geographically: 98% of people of European ancestry are wet and stinky, while essentially all Koreans and most Asians generally are dry and odorless. In a nice double-header of genetic determinism plus medical Eurocentrism, Medical News Today bowdlerized the story as, “Two percent of people have armpits that never smell.” Of course, other things besides ABCC11 can make you smell bad. Given sufficient antipathy to bathing and/or doing laundry, anyone’s armpits (and everything else) will begin to reek. And it takes a remarkably blinkered perspective these days to report this result as two percent of people—to neglect the roughly 4/7 of the world population that is Asian. The whole thing makes me break out in a cold sweat.

 

Anthill Anarchy

Two more papers made claims that were more than skin-deep. A paper in Nature, not on humans but on fire ants, suggests the existence of a “social chromosome.”  A string of 616 genes was identified that correlates with the type of social system an individual ant will accept: either a single-queen system or a multi-queen system.

If all the workers in a colony carry the B variant only, they will accept a single queen that also carries only the B variant (marked as BB, because the chromosomes come in pairs). But if some workers in the colony carry the b version of the chromosome, the colony will accept multiple queens — but only those queens with a mismatched “Bb” set of chromosomes. From the Roman Empire to Occupy Wall St., with the flip of a switch.

In the 1960s, during the first flowering of human cytogenetics, the finding that a disproportionate number of inmates in a British hospital for the violently insane carried an extra Y chromosome led to the idea of the “criminal chromosome.” So-called XYY males were branded as potential criminals. These unfortunates, it was speculated, were predisposed to violent crime as a result of having an extra dose of maleness, with its attendant propensities toward aggression and lack of empathy. Several serial killers were labeled as XYY (incorrectly, in most cases) and the “my genes made me do it” defense was attempted in court, though never successfully. The XYY controversy made headlines through the late 1960s and early 1970s, particularly when the science-activism group Science for the People got hold of a Harvard study intended to interrogate this and other claims about the effect of extra sex chromosomes on behavior. The controversy died when the research arm of the Harvard study was suspended. Thus ended this particularly primitive version of the fantasy of preventing violent crime by identifying it before it starts by aborting affected fetuses (bg essay). More sophisticated versions would involve large complexes of genes and subtler therapies; medication, say, and counseling, perhaps lifelong.[1]

The implications of the ant study also lie in the area of behavior control, though the present work limits its conclusions to entomology. “Our discovery could help in developing novel pest-control strategies,” said paper co-author Yannick Wurm (I know, I know) of the University of London. For example, a pesticide could artificially deactivate the genes in the social chromosome and induce social anarchy within the colony.” What could possibly go wrong?

 

Gene for humanity

Another new study identified microRNAs–short strings of nucleic acid that regulate gene expression–that are found in human brains and (so far) only in human brains. The blog Why Evolution is True delivers a sober account of the finding: “We have a human-specific molecule, miR-941, that regulates gene expression in our brains, and some of the genes it might have regulated have dropped out of the pathway.”

This modest but interesting finding has been overblown in the media to a “gene for humanity,” says whyevolutionistrue. The term “holy grail” really should be used only in conjunction with killer bunnies but the phrase’s mytho-comic connotations are apt here, I think. How thrilling (and frightening) to think there might be a single gene that holds the key to separating us from the apes! Could a single wayward x-ray to the groin lead to a Cro Magnon blessed arrival, fruit of the loins of a middle-class mom from Dubuque? Could we, by means of genetic engineering and maternal surrogacy, resurrect an extinct humanoid species such as, say, a Neandertal?

 

Search for the root causes of the search for root causes

As always, there are two distinct but connected forces at play in these stories. Gene-for hype occurs on at least two levels. First is the scientific fascination with seeking the hereditary component of anything. The laudable emphasis today on multi-gene complexes and gene-environment interaction has done little to dampen our enthusiasm for seeking the genetic “roots” or “basis” of natural behaviors. The reasons for this are complex, but at least part of the explanation is inherent in the science. Quite simply, environmental influences are hard to analyze using existing scientific methods. So the cutting edge of behavioral research brackets the environment and asks questions that are answerable (and of course fundable). This de facto determinism is built into the style of scientific practice: what counts as interesting is shaped by what is convenient to study.

Second, as scientific results filter outward from the lab to the media outlets and blogs to the public eyeball, the natural and necessary distillation of complex, nuanced findings into plain, sixth-grade-level language easily becomes perverted. How many hits would you get by writing, “Genes regulated by human-specific molecule may have dropped out of cascade pathway thousands of generations ago”? Perhaps the more relevant human-specific trait here is the desire for simple explanations and sensational stories about root causes and “the key” to whatever.

It is tempting to write that this impulse for ultimate causation explains everything about genetic determinism. But that would create more problems than it solves.

[1] Court Brown, W. M. “Sex Chromosomes and the Law.” The Lancet 280, no. 7254 (1962 1962): 508-09; Maclean, N., J. M. Mitchell, D. G. Harnden, Jane Williams, Patricia A. Jacobs, Karin A. Buckton, A. G. Baikie, et al. “A Survey of Sex-Chromosome Abnormalities among 4514 Mental Defectives.” The Lancet 279, no. 7224 (1962 1962): 293-96; Jacobs, Patricia A., M. Brunton, M. M. Melville, R. P. Brittain, and W. F. McClemont. “Aggressive Behavior, Mental Subnormality and the XYY Male.” Nature 208 (1965 1965): 1351-52. doi:10.1038/2081351a0.

Walzer, S., and P. S. Gerald. “Social Class and Frequency of XYY and XXY.” Science 190, no. 4220 (1975 1975): 1228-9; Steinfels, M. O., and C. Levine. “The XYY Controversy: Researching Violence and Genetics.” Hastings Cent Rep 10, no. 4 (1980 1980): Suppl-1-32.