Tag Archives: genes for

Stop saying “biologically programmed,” goddamit!

Here’s your quick daily dose of biological determinism. This is nice because it combines deterministic thinking about both genes and brains. If this article were a bird it would be a Great Blue Heron–not exactly rare, but impressive nonetheless. I’m going to pick on it, largely because I slept like crap last night and I’m feeling cranky.

US News and World Report asks, “Could a gene help make you obese?” Okay, that right there is either shocking (You mean it’s not just eating too much?) or trivial (No shit. Genes could and indeed do help in making me everything I am).

People who carry two copies of a variant form of the “FTO” gene are more likely to feel hungry soon after eating a meal, because they carry higher levels of the hunger-producing hormone ghrelin in their bloodstream, an international team of scientists found.

Holy crap! There’s a hunger-producing hormone? Bip! Bip! Bip! “Hello, World Health Organization? Yea, look, this is gonna sound crazy, but we can END WORLD HUNGER TOMORROW! Seriously! All we need is four tanker-freighters of anti-ghrelin…”

What’s more, brain scans revealed this double FTO gene variant changes the way in which the brain reacts to food and ghrelin.

Oh god, where’s the Alka-Seltzer? I knew I shouldn’t have had that third plate of deep-fried ghrelin poppers before the game last night. Probably why I slept so crappy…

And now we come to the neuro-determinism part of the post.

People with the double variant displayed different neural responses in the brain region known to regulate appetite and the pleasure/reward center that normally responds to alcohol and recreational drug use.

I don’t have a problem with referencing the nucleus accumbens, the so-called “pleasure center.” That research is decades old. But the phrasing here subtly and repeatedly encourages the crass phrenological misperception that the brain is just a bunch of lumps each dedicated to some 21st century activity, like chugging Jaegermeister, snorting Adderall, and swallowing whole Twinkies. It’s not, people. The genome doesn’t work like that and the brain doesn’t work like that. It seems that way, because we study them by trying to figure out how brains and genes influence stuff we already do. When you look from the bottom up at how they work to produce signals, it turns out to be much more complex and subtle.

“Oh, but Genotopia,” the journalist complains. “I can’t go on about the nucleus accumbens! I know it’s a simplification, but these little short-cuts are necessary in order to write about complex science for wide audiences!”

Okay, whiner, I’ll do it for you. Ta-da:

People with the double variant displayed greater activity in two key brain regions, one involved in creating the sensation of hunger, the other linked to feelings of pleasure.

You see? Easy. A couple of little tweaks and you introduce hints of contingency and inter-connectedness, rather than implying that we’re all made out of Legos. No waffling, and no Latin.

Just so the poor writer doesn’t feel singled out, the scientists do it too. The lead author on the study says,

 “What this study shows us is that individuals with two copies of the obesity-risk FTO variant are biologically programmed to eat more.”

Really? You’re going to go with “biologically programmed”? I thought we got rid of that language just after Jurassic Park. People homozygous for this one variant may well show a statistical correlation with obesity. It may even be legitimate to say they have a predisposition to eat more. But for Mendel’s sake, ban the cyborg-speak, will you?

Okay, I have to get to work, so I’m not going to go through this entire article. But look, this is an increasingly important issue. We are constantly being told how we have to take our healthcare into our own hands. Education is crucial. And the single most important concept in dealing with the really complex systems of the body–the genome, the brain, the immune system–is probability. By 2013, deterministic speech like this is just laziness. Good science writers and careful scientists don’t say this stuff any more. Doing so is a real disservice to a public that is increasingly dependent on translations of science for its understanding of biology and health. Trash those old metaphors, adopt a few new clichés and stock phrases, and we will be a long way toward a healthier understanding of our own bodies.

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

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.