Tuesday, March 13, 2012

Evan Charney's Critique of Genopolitics and the Genetic Paradigm

The two most common reasons for rejecting biopolitical science arise from misconceptions about the biological study of animal behavior. 

The first reason is the assumption that any biological explanation of political behavior must be unreasonably reductionistic and deterministic.  This is mistaken, because it ignores the fact that biological science must recognize the individuality, the contingency, the complexity, and the historicity of animal behavior.

The second reason is the assumption that while animal behavior shows a fixity as determined by genetic instincts, human behavior is unique in its flexibility because of its openness to social learning and individual judgment and its freedom from genetic influence.  This is mistaken, because other animals--even those that seem very simple--show a flexibility in their behavior that is similar to human behavior in being constrained but not determined by genetics.

Both of these points can be clarified by considering the current debate in political science over "genopolitics."

In recent years, some political scientists in the biopolitics movement have tried to show how human genetics might influence political behavior.  One prominent example is the article by John Alford, Carolyn Funk, and John Hibbing in 2005, in the American Political Science Review, which argued that twin studies showed that propensities towards "conservatism" or "liberalism" were strongly influenced by genetics.  In response, Evan Charney criticized this article for its unwarranted genetic determinism.  In a previous post, I commented on this debate, arguing that it displayed too much straw-man argumentation based upon a false dichotomy of nature versus nurture.

Now, Charney has renewed this debate, and this time, he's criticizing an article by James Fowler and Christopher Dawes.

In 2008, The Journal of Politics published an article by Fowler and Dawes entitled "Two Genes Predict Voter Turnout."  Here's the abstract for the article:
Fowler, Baker, and Dawes (2008) recently showed in two independent studies of twins that voter turnout has very high heritability.  Here we investigate two specific genes that may contribute to variations in voting behavior.  Using data from the National Longitudinal Study of Adolescent Health, we show that individuals with a polymorphism of the MAOA gene are significantly more likely to have voted in the 2004 presidential election.  We also find evidence that an association between a polymorphism of the 5HTT gene and voter turnout is moderated by religious attendance.  These are the first results ever to link specific genes to political behavior.
These two genes--MAOA and 5HTT--influence the metabolism of serotonin in the brain.  Some studies suggest that the serotonin system affects social behavior, in that high levels of serotonin tend to promote prosocial behavior, while low levels tend to promote antisocial behavior.  Some of these studies suggest that there is an interaction of genes and environment, so that, for example, those individuals genetically endowed with an efficient serotonin system are better able to respond to stressful life events without becoming persistently depressed, or better able to experience abuse as children without becoming abusive as adults.  

Since many social scientists have explained voter turnout as a prosocial behavior, Fowler and Dawes hypothesize that genes favoring high levels of serotonin will promote prosocial behavior and thus promote voter turnout.  They found that the allele of the MAOA gene promoting efficient metabolism of serotonin was directly associated with voter turnout.  But they also found that the allele of the 5HTT gene promoting efficient metabolism of serotonin favored voter turnout only when the individuals with this allele frequently attended religious services.  Social scientists have noticed that people active in religious organizations tend to show higher rates of voting, and this seems to be the case here.  So here there's an interaction between genes and environment.

That two genes predict voter turnout is an astonishing claim.  But while they make this claim, Fowler and Dawes also qualify, if not contradict, this claim in their article.  They say that environment might be more important than genes for voter turnout, and they indicate that the two genes they have studied raise the likelihood of voting by only 5% to 10% (588).  So now it seems that while these two genes have some influence, their influence is so weak that they cannot predict voter turnout.

They stress the weakness of this influence in the last paragraph of their article: "It is important to emphasize that there is likely no single 'voting gene'--the results presented here suggest that at least two genes do matter and there is some (likely large) set of genes whose expression, in combination with environmental factors, influences political participation" (590).

So their final conclusion seems to be: these two genes do matter, but they probably don't matter very much in causing voting behavior.

This points to some of the problems with genetic explanations of political behavior identified by Evan Charney.  In the March 2012 issue of the American Political Science Review, Charney and William English have an article entitled "Candidate Genes and Political Behavior," which criticizes the article by Fowler and Dawes.  Charney and English make two kinds of arguments.  First, they argue that, if one considers four kinds of methodological problems, one can see that the data set used by Fowler and Dawes does not show that two genes predict voting behavior.  Second, they argue that in general there are many difficulties in any attempt to identify particular genes as causing social behavior.  This second more general argument is part of Charney's criticism of what he has called the "genetic paradigm," which he has elaborated in an article to be published in Behavioral and Brain Sciences.

Charney and English identify methodological problems in four areas--phenotype specification, population stratification, genotype classification, and independence of cases and controls.  Rather than going into the details of their analysis, I will only suggest that one sees in their debate with Fowler and Dawes the same fundamental difficulty that arises in Charney's debate with Alford, Funk, and Hibbing.

In both of these debates, the opposing sides employ the rhetoric of arguing against a "straw man."  Charney criticizes his opponents for being genetic determinists.  His opponents criticize him and others like him for being environmental determinists.  And yet no one here is defending either genetic determinism or environmental determinism.  Charney agrees that genes matter.  His opponents agree that environment matters.

The debate over the Fowler and Dawes article is confusing, because Fowler and Dawes imply two different kinds of claims--one is very astonishing and the other is very modest.  The very astonishing claim is that two genes predict voter turnout, and this is the claim that Charney easily refutes.  The very modest claim is that these two genes might matter a little in influencing voter turnout, but these two genes by themselves cannot actually predict voter turnout, and in fact these two genes are probably much less important than other factors.  Charney comes close to agreeing with this very modest claim when he says: "DNA is one component of a complex, integrated, interactive, and dynamic biological-environmental-ecological process through which biological organisms come to manifest divergent phenotypes."  Charney, Fowler, and Dawes all agree that particular genes influence but do not specify behavior, because genes interact with other genes, with other biological factors, and with the physical and social environment.

In his APSR article, Charney has a section on "Broader Issues in Genetics," which briefly summarizes arguments that he has elaborated in his BBS article entitled "Behavior Genetics and Post-Genomics."  This BBS article makes clear the profound implications of Charney's position. 

Biological research over the past 20 years has uncovered evidence that some of the most fundamental assumptions of modern genetics are dubious, and a few biologists are suggesting that this requires a "paradigm shift" in how we understand genetics and biology generally.  The great value of Charney's paper is that he summarizes this research in order to force us to reexamine the "genetic paradigm" of behavior genetics.  Those of us who belong to the biopolitics movement will have to respond to this challenge.

Much of what Charney says constitutes the "genetic paradigm" is captured by the six basic assumptions of behavior genetics--three for heritability studies (HS) and three for gene association studies (GAS).  Heritability studies use adoption studies and twin studies to determine the proportion of phenotypic variance in a given population that can be attributed to genotypic variance.  Gene association studies look for statistically significant associations between particular genes and particular phenotypic traits.  The Alford, Fund, Hibbing (2005) article is an example of a heritability study.  The Fowler and Dawes (2008) article is an example of a gene association study.

Here is how Charney states the six basic assumptions:
HS1. 100% of the genes of MZ [monozygotic] twins are genetically identical; on average, 50% of the genes of DZ [dizygotic] twins are genetically identical.  On average, 50% of the genes of non-twin siblings are genetically identical.

HS2.  The percentages of genetic identity in HS1 never change (i.e., they are unvarying).  That is, MZ twins, from conception to death, are always 100% genetically identical; DZ twins are always ~50% genetically identical; non-twin siblings are always ~50% gentically identical (heritability, however, can change over the life course).
HS3.  All causes of phenotypic variation that impact human behavior can be attributed to a latent genetic (G) or environmental (E) parameter, or the interaction of the two (G x E).

GAS1.  Persons have identical DNA in all of the cells and tissues of their bodies (with the exception of germ cells, red blood cells, and certain cells in the immune system).
GAS2.  The presence of a particular genotype (polymorphism or mutation) entails that it is "turned on," that is, it is capable of being transcribed in a manner associated with that polymorphism or mutation.  Hence, the same two polymorphisms in any given two individuals will have the same capacity to be transcribed in the same manner (precisely what this entails will be considered below, but it emphatically does not mean that any two polymorphisms in any two individuals are always being transcribed to the same extent).

GAS3.  Specific genes are coded for the production of specific proteins.
Charney's argument is that recent research casts doubt on all of these assumptions.

Identical (monozygotic) twins are not really genetically identical.  For example, we now know that a large portion of the human genome consists of transposable elements--repetitive DNA sequences that can move from one location to another--that have been called "jumping genes."  These "jumping genes" seem to be especially common in the human brain.  Some researchers believe that this is one major reason why individuals have unique brains, including identical twins.

We also know that individuals, including twins, are unique because of copy number variations in DNA--stretches of DNA present in multiple copies and showing high variation between individuals.  Moreover, this variation occurs not only between individuals but also within individuals, so that--contrary to GAS1--the DNA is different in different cells of the same body.  This is one source of "mosaic genomic variation."

Another source of variation between and within individuals is variation in the number of chromosomes--"aneuploidy."  Some human individuals have more or less than the 23 pairs of chromosomes that we assume to be normal.

Contrary to GAS2, genes are not self-activating, because whether they are activated depends on epigenetics--the complex system of modifications of the genome that determine whether genes are turned on or off in response to environmental input.  Moreover, these epigenetic modifications can be inherited, which constitute a form of Lamarckian inheritance of acquired traits.

This genetic and epigenetic heterogeneity comes from within germ cells, from the prenatal environment of the mother's body, and from the postnatal environment.  At all three levels, the behavior of a mother can influence the genetic and epigenetic constitution of her offspring in ways that are heritable.  For example, a nurturing mother induces changes in her child that can be passed on to her grandchildren.

The postnatal environments of monozygotic twins induce genetic and epigenetic changes through differences in life experiences.  For example, if one twin exercises a lot, and the other does not, the exercising twin can experience increased production of new neurons in the hippocampus.

Contrary to the assumption (AS3) that specific genes are coded for the production of specific proteins, we know that a single gene can code for many different proteins.  Not only does each gene have multiple effects, but also each gene interacts with many other genes to generate complex traits.

For these and other reasons surveyed in Charney's article, we cannot predict complex human phenotypes--like political ideology or voting behavior--from a human genotype.  The ultimate evolutionary reason for this is that human beings have evolved for phenotypic plasticity--the capacity to change one's phenotype in response to a highly complex and variable environment.

Many of us assume that this evolved capacity for behavioral flexibility is unique to human beings--perhaps a product of our uniquely large and complex brains.  And it is true that the behavioral flexibility that comes from the human capacities for language and symbolic reasoning probably is uniquely human.

But it is also true that most of what has just been said about the complexity, variability, contingency, historicity, and flexibility of genetic influences on behavior is true for many animals other than human beings--even animals as seemingly simple as nematode worms, fruit flies, and mice.  This confirms Charles Darwin's conclusion that "man is the modified descendant of some preexisting form" (Kendler and Greenspan 2006).

This research also confirms my claim--often made on this blog--that biopolitical science must be a complex science of emergent evolution that embraces not only genetic evolution but also the cultural history of political regimes and the individual history of political actors.  Human genetics constrains but does not determine human cultures and human judgments.

Something similar could be said about the political science of any political animal.  So, for example, Jane Goodall's Chimpanzees of Gombe explains the chimpanzee politics of the community at Gombe through the complex interaction of chimpanzee genetic nature, chimpanzee cultural traditions, and individual chimpanzee life histories and personalities. 

Just as is the case for human politics, the irreducible complexity and historical contingency of chimpanzee politics made it impossible for a primatologist like Goodall to make precise predictions about the future of the society at Gombe.  So, for example, she could make generic predictions about the need for a dominance hierarchy with an alpha male at the top, but she could not make specific predictions about which individual would fill that alpha position in the future.  There probably are a few chimp genes that show a statistically significant association with alpha dominance, but that association is probably too weak to support exact predictions.

My article on "Biopolitical Science" sketches a biological science of political animals that moves through three levels of deep political history--the universal political history of the species, the cultural political history of the group, and the individual political history of animals in the group.  Genopolitics would be one element of such a biopolitical science.

Some of my previous posts on related themes can be found here, here, here.here, here., and here.


Alford, John H., Carolyn Funk, John R. Hibbing, "Are Political Orientations Genetically Transmitted?" American Political Science Review 37 (1) (2005): 246-78

Arnhart, Larry, "Biopolitical Science," Politics and the Life Sciences 29 (March 2010): 24-47.

Baillie, J. K., et al., "Somatic Retrotransposition Alters the Genetic Landscape of the Human Brain," Nature, 470 (24 November 2011): 534-37.

Charney, Evan, "Behavior Genetics and Post-Genomics," Behavioral and Brain Sciences 35 (2012): 331-410.

Charney, Evan, and William English, "Candidate Genes and Political Behavior," American Political Science Review (March 2012).

Flint, Jonathan, Ralph J. Greenspan, and Kenneth S. Kendler, How Genes Influence Behavior (Oxford: Oxford University Press, 2010).

Fowler, James H., and Christopher T. Dawes, "Two Genes Predict Voter Turnout," The Journal of Politics, 70 (July 2008): 579-94.

Gage, Fred H., and Alysson R. Muotri, "What Makes Each Brain Unique," Scientific American, 306 (3) (March 2012): 26-31.

Greenspan, Ralph J., An Introduction to Nervous Systems (Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 2007).

Kendler, Kenneth S., and Ralph J. Greenspan, "The Nature of Genetic Influences on Behavior: Lessons for 'Simpler' Organisms," American Journal of Psychiatry, 163 (10) (October 2006): 1683-94.

1 comment:

Rebecca J. Hannagan said...

I took some time to consider the Charney article, the Dawes and Fowler article, and your commentary before posting my comment. Unfortunately I have nothing profound to offer as you have addressed the "straw man" issue here. My comments have more to do with the role of professional journals in academic exchange and the quality of both.
Here is my concern: the APSR is the flagship journal of our discipline. Everyone holds it in the highest esteem and considers an article in it to be the paramount of any political scientists' career. The idea is that it is so difficult to publish in the APSR and the work so compelling, excellent, and "moves the discipline forward" that it truly takes profoundly excellent work, or years of publishing elsewhere to gain the reputation of work that matters to political science to finally reach this pinnacle and be published in the APSR. Now, having only been a card carrying political scientist for about 5 years I can only speak to what I have been told and what I have observed. I am sure that over the years the APSR has ebbed and flowed in its quality due to the editors, editorial board, and quality and volume of submissions. That being said, I do not think I am alone in the perception that the APSR is THE journal to publish in and that the competition is the fiercest it has ever been. Thus, why was this article the lead article in the APSR?
Here are my thoughts on the matter. Genopolitics, biopolitics, or twin studies or gene association methods are sexy. Period. Charney's critique of Alford, Funk and Hibbing was written with a kind of fever pitch to leave one with the feeling that the sky of political science was falling. (Coincidently I wrote a response to that article that was published as a small symposium in Perspectives - my co-author and I argued that this work had been done for a very long time elsewhere and was the natural progression of investigation in our discipline). Charney's critique of Dawes and Fowler is less intense, but the same sentiment is there. I do not detect the basis of a firmly grounded epistemological issue with biopolitics or genopolitics, or whatever we are calling it these days. This is mere wrangling about measurement, but again, as you clearly state in this blog entry, it is moot because Dawes and Fowler do not take anything near a hardline on genetic determinism. To my knowledge, no one does. So why is this the lead article in the top journal of our discipline? What are we disagreeing about? Is this just silly academic exchange? Is Charney just enterprising enough to make his career out of critiquing the folks doing the "sexy" new work? That is perfectly fine with me. I think academic banter is fun. There are plenty of outlets to publish academic banter.
What is not fun is reading an APSR article and thinking that not only did I not learn anything, but that what is disguised as a very important critique of a body of work is nothing of the sort. This is not promoting intellectual exchange. Knowledge of the discipline has not been pushed forward. In short, what are you doing APSR?