Anti-determinism on the march!

Nice piece today from SciCurious, guest blogging over at Scientific American. The post is an analysis of a recent article in Nature claiming that by knocking out serotonin in two different ways (both neurotransmitter production and receptors), they abolished sexual preference. The mice apparently mounted either sex with equal frequency.

SciCurious does a beautiful job dissecting the assumptions in the Nature article, analyzing the data, presenting alternative hypotheses, and looking at the history of the research. For example, the authors might have merely lowered the threshold of sexual activity–an extension of “all girls get prettier at closing time”. Or perhaps the researchers influenced the perception of other cues, for example olfactory cues. “So does this paper prove that there are drastic increases in sexual behavior associated with low serotonin?,” SciCurious writes. “Absolutely. Does it show that low levels of serotonin change sexual PREFERENCE? Well, that’s difficult to say.”

Also, Ed Yong looked at the article from a different but equally skeptical point of view. He points out how difficult it is to translate these kinds of behavioral findings from mice to humans. Further, he writes, “serotonin isn’t all about sex.” When I was a teaching assistant for the Neural Systems and Behavior course at Cornell back in the late 1980s, we used to drill in to the students’ heads the idea that neurotransmitters do not have behaviors. They act in many regions of the brain and influence all sorts of behaviors in ways that are very far from straightforward.

Yong worries (rightly) that anti-gay groups will use findings like this to argue for a simple biological basis for homosexuality, perhaps even proposing serotonin therapy as part of their effort to “cure” it. And SciCurious links to news stories soon appeared suggesting that the researchers had “turned mice gay.”

Such stories illustrate a fundamental fallacy that is one of the gravest dangers of popularizing science. For the sake of argument, let’s say the researchers did in fact eliminate sexual preference. In what sense is “no sexual preference” the same as “gay”? Ans: only in a world so normative that strict, unwavering heterosexuality is the only behavior considered normal. Of course, there are lots of people like that–I read about them all the time. But it is blinkered, naive, and deeply chauvinistic.

Biological and especially genetic explanations of behavior are a double-edged sword. The gay community has oscillated in its support for research to find “gay genes” and other traces of the biological basis of homosexuality. If homosexuality is innate, the reasoning goes, then it is cruel and pointless to try to “cure” gays, in the same way it was cruel to “cure” left-handed people.

But “gay” is a cultural construct. There were no “gays” in Ancient Rome or in 19th century Paris, and there are no gays in the Foré of Papua New Guinea. Here and now, in our culture, we need the term in order to protect human rights that are trampled on by people unreflectively absorbing an outdated cultural taboo on homosexual activity. But in the long run, the ideal should be to get rid of the concept–for us all, in short, to be “gay-blind.”

Good skeptical science writing helps that cause, because it exposes fallacies in the ways we think about science. I’m fine with describing a physiological mechanisms for a behavior, but we need to be careful not to equate mechanism with cause. I’m wary of science writing that talks about the “roots” or the “basis” of complex behavior or disease. It implies a hierarchy that blinds us to many biological mechanisms that work in the other direction. In biology, cause and effect go both directions: behavior changes gene activity as much as gene activity changes behavior. Studies purporting to examine the biological “basis” of behavior rely on cross-species analogies and make unsupportable assumptions about motivation.

In short, a “gay” mouse is a ludicrous concept.

 

 

Thalassophilia unmasked

There is no gene for thalassophilia—yet, anyway.

My satirical post last week about scientists finding a gene for love of the sea was intended to make a point about how we view genomics today—and a historical point about how we smugly congratulate ourselves on being so much more sophisticated than early human geneticists and eugenicists. Most people got that it was a spoof, but I thought it would be worthwhile to discuss some of the deeper issues at stake.

Charles Davenport was a real scientist, and the quotes from him are real. Davenport was a geneticist in the first half of the 20th century and the leader of the American Eugenics movement during the Progressive Era. He is often demonized as wrong-headed, misguided, and simple-minded. Indeed, he could be all of these things. Davenport really did believe there was a recessive, male-linked trait for the love of the sea. Thalassophilia has become a classic example of how eugenicists could ignore obvious environmental explanations in favor of the hereditary. When I told my 11-year-old daughter about Davenport’s thalassophilia, she immediately saw the fallacy: the sons of ship captains learn their love of the sea, they don’t inherit it.

My larger point is that simplistic analyses like Davenport’s can be masked by numbers and fancy technology.

For years, medical genetics involved the search for genes underlying genetic disease. Diseases that were caused by a defective gene, and not, say, by a germ or some other environmental factor. But that distinction has been erased. We used to think of genetic traits and non-genetic traits. Now, non-genetic traits are called “complex”—i.e., partly genetic and partly environmental. In other words, all diseases, and indeed all traits are understood as partially genetic.

There are sound reasons for thinking this way. I’m not arguing that those genes don’t exist. I don’t question the data—I’m happy to believe that there really is a genetic association with all of these traits. Indeed, I think it’s becoming possible to find a real, verifiable genetic basis for almost anything you like.

The advent of genome-wide association studies (GWAS) has made it vastly easier to examine traits with smaller and smaller genetic contributions. In essence, you can pick your trait, sample the DNA of a large group of people, and scan their genomes for bits of shared sequence.

As a consequence, we have the recent bloom of studies describing the genetic component of all sorts of “complex” traits, from religiosity to getting drunk and beating people up. We’re only limited by our imaginations, and by the kinds of traits we’re interested in today.

Thinking about these recent studies, it occurred to me that these traits were not fundamentally different from Davenport’s old favorite, thalassophilia. I bet, I said to myself, that if sailing were as culturally important today as it was in 1919, people would be doing GWAS to find the genetic basis of sea-lust. And I bet they’d find it.

Of course, there are big differences between human genetics in 2011 and human genetics in 1919. Davenport advocated sterilization laws and immigration laws to manage and shrink what he saw as the swelling populations of the “unfit.” That would be inconceivable today. I don’t think we’re returning to a “new eugenics” in any meaningful sense.

But cutting across the cultural differences are some continuities. One of them is the desire to believe there is a simple genetic explanation for our tastes and talents. That I think is a dangerous view. So on the one hand, I think we should be careful to evaluate 1920s science by the standards of the day, rather than by those of the 21st century. And on the other, we must not delude ourselves that modern science is completely objective. Mechanistic explanations are not proof against cultural bias.

My spoof was intended as a word of caution, a way to inject a note of skepticism about genetic explanations of human nature. C.M (“Call Me) Ishmael, the journal Genetic Determinism Today, MysticGene, the 4C (“for sea”) variant, the salt-stained polo shirts and the sailing widows—all that was pure balderdash. As the motto of this site goes, “Here lies truth”— in roughly equal measure.

So, keep your heads up, folks—and watch for the keyword “Satire” in the Categories section of this blog. Thanks for reading.

Scientists find gene for love of the sea

What did Thor Heyerdahl, Captain Ahab, and Odysseus have in common? They all may have shared a common variant of a gene for love of the sea.

Researchers at Mystic University in Connecticut have identified a gene associated with seafaringness, according to an article to be published tomorrow in the journal Genetic Determinism Today. Patterns of inheritance of the long-sought gene offers hope for “sailing widows,” and could help explain why the sailing life has tended to run in families and why certain towns and geographical regions tend historically to have disproportionate numbers of sea-going citizens.

The gene is a form of the MAOA-L gene, previously associated with high-risk behavior and thrill-seeking; another form of the gene, found last year, made news as the “warrior gene.” The current variant, dubbed 4C, was found by a genome-wide association study (GWAS) on 290 individuals from Mystic, CT, New Bedford, MA, and Cold Spring Harbor, NY—all traditional nineteenth-century whaling villages. Residents showed the presence of the 4C variant at a frequency more than 20 times above background in neighboring landlocked towns.

C. M. Ishmael, the lead researcher on the study, said the findings could be a boon to medicine. Although the International Whaling Commission outlawed commercial whaling in 1986, the research could benefit literally hundreds of “sailing widows” left alone for Wednesday-evening sailboat races up and down the East Coast. Each year, an average of 11 salt-stained Polo shirts wash up on the New England and Mid-Atlantic coasts, the only remains of lantern-jawed investment bankers and their half-million-dollar boats. Ishmael said he is trying to have the irrational urge to sail entered into the Diagnostic and Statistical Manual, standard reference for psychiatric diseases, in the next, fifth, edition.

“This receptor is an exciting potential target for new drug therapies,” Ishmael said in a phone interview. “We hope lots of companies will be interested in it. And venture capital, too.” Ishmael is himself CEO of a company, MysticGene, formed to develop such therapies. When asked about potential conflict of interest, he replied cryptically, “Well, duh.” Shares of MysticGene closed higher on Monday following the announcement.

The gene for seafaringness has long been an object of study for human geneticists. The trait was first described in 1919 by Charles Davenport, director of Cold Spring Harbor Laboratory, who named it “thalassophilia.” Using pedigree analysis and anecdotal correlation, Davenport identified thalassophilia as a sex-linked recessive gene and distinguished it clinically from wanderlust, or love of adventure. Although one might think naively that people living in towns with good harbors would tend to go to sea, Davenport suggested the reverse: those with the thalassophilia trait have tended to migrate toward regions with good harbors and found settlements there. The current study does nothing to refute Davenport’s analysis.

Further, a tentative expansion of the GWAS analysis to various racial groups largely confirms Davenport’s observations that thalassophilia is more prevalent in Scandinavians and the English, and less common in people of German ancestry.

Thalassophilia joins a rapidly growing list of complex behavioral traits that have been shown to have a genetic basis, thanks to GWAS. Besides the warrior gene, recent studies have found genetic links to promiscuity, aggressive behavior, especially while drinking, religiosity, and bipolar disorder, or manic depression—all traits that Davenport and other early human geneticists were deeply interested in. The difference is that modern science better understands the mechanisms involved.

“Seamen know very well that their cravings for the sea are racial,” Davenport wrote in 1919. “’It is in the blood,’ they say.” Today we know it’s not in the blood—it’s in the genes.

The true bits:

Garland E. Allen, “Is a New Eugenics Afoot?,” Science 294, no. 5540 (October 5, 2001): 59 -61. (http://www.sciencemag.org/content/294/5540/59.short)

Charles Benedict Davenport and Mary Theresa Scudder, Naval officers: their heredity and development (Carnegie Institution of Washington, 1919),http://books.google.com/books?id=EWESAAAAYAAJ&dq=naval%20officers%3A%20their%20heredity%20and%20development&pg=PP1#v=onepage&q&f=false.

Richard Alleyne, “A gene that could explain why the red mist descends,” Telegraph.co.uk,http://www.telegraph.co.uk/science/science-news/8219521/A-gene-that-could-explain-why-the-red-mist-descends.html.

Jeremy Taylor, “Violent-drunk gene discovered,”http://www.asylum.com/2010/12/23/bad-drunk-gene-discovered/.

Justin R. Garcia et al., “Associations between Dopamine D4 Receptor Gene Variation with Both Infidelity and Sexual Promiscuity,” ed. Jan Lauwereyns, PLoS ONE 5, no. 11 (11, 2010): e14162.

C. Frydman et al., “MAOA-L carriers are better at making optimal financial decisions under risk,” Proceedings of the Royal Society B: Biological Sciences (12, 2010),http://www.newscientist.com/article/dn19830-people-with-warrior-gene-better-at-risky-decisions.html.

 

 

First post

Hello and welcome!

I’m glad to be the newest member of the ScienceBlog team. I am going to be writing mainly on genes,  genomes, heredity, and health. Subjects in the news today such as personal genomics, pharmacogenomics, and genetic screening and counseling all have strong historical roots. Examining them can really cut through the hype and illuminate the headlines. I’m going to try to add some depth and perspective–and hopefully some humor–to biomedical questions that affect us all.

Factlets: I’m on the faculty of Johns Hopkins University, where I teach courses on 20th century biomedicine, the history of genetics, and oral history. I have two degrees in biology and one in history. I’ve written a book on the geneticist Barbara McClintock and edited one on the Intelligent Design controversy. My current book project is a history of medical genetics. The working title is The Science of Human Perfection and it will be published by the good folks at Yale University Press.

I also like to write for wider audiences. I’ve published in the New York Times Book Review, Natural History, Science, New Scientist, and The Believer, and have been on National Public Radio.

I also blog over at the Philadelphia Area Center for History of Science, where I’m planning to focus on more historical, probably somewhat more scholarly material. I tweet @nccomfort and you can find some of my writings on academia.edu.

Okay, enough preamble. Let’s get started!