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Have researchers really discovered any genes for behavior? Candidates welcome

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double helixA couple of science-writing colleagues objected to my recent post on the "warrior gene." Both accuse me of throwing the baby of modern behavioral genetics—which seeks to link complex behavioral traits to specific genes—out with the bathwater of media hype. Naturally, my innate bellicosity compels me to respond.

My warrior-gene post examined the reported association between aggression and MAOA-L, a variant of a gene that helps produce the enzyme monoamine oxidase-A. The journal Science dubbed MAOA-L the "warrior gene" back in 2004 and the name stuck. Ed Yong, the British blogger, says in a comment to my column that just because some folks sensationalize the MAOA-aggression link doesn’t mean it’s bogus.

Ed explains that "children who carry MAOA-L AND come from abusive homes have a higher risk of aggressive behavior; that’s not true if they come from more stable backgrounds. Likewise, the hot sauce experiment found that people with MAOA-L are more likely to mete out punishment when they are provoked—another case of nature via nurture. It’s sad that the fascinating area of gene-environment interactions isn’t discussed at all" in my post.

Ed focused on these "gene-environment interactions" in his 2010 article, "Dangerous DNA: The Truth about the ‘Warrior Gene.’" Ed cautioned that MAOA-L "is not a gene ‘for’ aggression," but he accepted the notion that MAOA-L plus certain environmental stimuli raises the risk of aggression. First of all, the hot-sauce study found a minute difference, at best, between the MAOA-L subjects and those carrying the more common MAOA gene. That’s why I didn’t find it credible.

Ed also touted a 2002 report in Science by Avshalom Caspi of King’s College, London, and seven colleagues that MAOA-L carriers were more likely than non-carriers to display antisocial behavior, but only if they were "maltreated" as children. What Ed doesn’t say is that two studies by geneticists at the University of Colorado have failed to confirm the Caspi claim; you can read these reports here and here. Did they get any attention? Of course not. This has been the pattern of media coverage of behavioral genetics since I started following it in the late 1980s: The spectacular claim makes headlines, and the counter-evidence doesn’t. The public and even many journalists and scientists are left with an erroneous impression that behavioral genetics is explaining more and more of what we do.

I’ll call the other journalist who knocked me, who prefers to remain nameless, Ed2. He accused me of pulling a "bait and switch," in which I conflated "pop misuses of the ‘warrior gene’" with the overall performance of behavioral genetics, which deserves more respect. When I asked him for examples of robust linkages of specific genes to complex behavioral traits, Ed2 gave me two.

One is research linking Lesch-Nyhan disease, a rare disorder affecting one out of every 380,000 people, to a gene called HPRT. Lesch-Nyhan causes over-production of uric acid, which results in painful buildup of uric acid crystals in joints, the urinary system and subcutaneous tissue. Sufferers sometimes strike and bite themselves, even gnawing off their own fingers. Lesch-Nyhan is clearly not a behavioral disorder but a physiological disease with behavioral side effects. Ed2 was pulling a bait and switch on me!

Ed2′s other example is a 2010 paper linking the gene CMYA5 to schizophrenia, which unlike Lesch-Nyhan has no definitive physiological symptoms and so counts as a complex behavioral disorder. The CMYA5 study looks impressive; it involved a huge team of researchers from dozens of institutions around the world examining more than 33,000 subjects. Reading the data-dense paper, I couldn’t figure out how much CMYA5 supposedly increases the risk of schizophrenia. I emailed the lead author, Sam Chen of Virginia Commonwealth University, and he told me that if you have the CMYA5 gene, your risk of schizophrenia increases by seven percent.

Let’s put this statistic in context. About one in 100 adults around the world are schizophrenic, which means that the risk of schizophrenia for the general population is 1 percent. If you carry the CMYA5 gene, your risk rises by an extra 0.07 percent to 1.07 percent, according to Chen. If you have a schizophrenic first-degree relative, such as a sibling, your probability of becoming schizophrenic is about 10 percent, which is more than 100 times the added risk of having the CMYA5 gene. My guess is that the finding of Chen et al. will eventually be discarded as just another false positive, like all the other alleged "schizophrenia genes" dating back more than two decades. But if even if the correlation holds up, what good is it? Is research like this really worth the effort?

When it comes to behavioral genetics, so far there is no baby; there’s only bathwater.

Image courtesy Wiki Commons


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  1. 1. Archimedes 11:25 am 05/2/2011

    The behavior of living organisms is determined by both heredity and environment. This is a settled scientific fact which, as it has in the past, faced aggressive and hostile opposition from a variety of political, scientific, religious, and other groups and individuals.
    My Mendelian and Darwinian theory, which is even more controversial, is that some changes in human behavioral changes are triggered by environmental circumstances triggering genetic markers which catalyze character, intellectual, and personality changes. Natural warriors, therefore, emerge in the appropriate environment. Mental illness for particular individuals results from environmental circumstances which trigger specific genes. Affection for a particular woman by a man may result from the same. In fact, studies have shown that men are more attracted to women from their particular ethnic group (genetic triggering of the same). A scientific theory which is supported by a wide variety of evidence and is reproducible, such as the aforementioned, is further proof in support of those Darwinian, Mendelian, and other scientific theories long accepted by majority but which remain "politically incorrect" to those who reject scientific reasoning.

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  2. 2. mem from somerville 7:07 pm 05/2/2011

    Didn’t they find behaviors associated with Williams Syndrome? I am having trouble with OMIM right now so I can’t get the details. Will keep looking.

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  3. 3. FOOZLER8 6:16 pm 05/3/2011

    What’s the difference? If a behavior or behavioral pattern is the result of a disease or just ‘normal’ physiology the result is the same.

    We aren’t likely to find too many single genes producing behavioral patterns, which tend to be complex as a result of being produced by more than one gene.

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  4. 4. dubina 3:48 am 05/4/2011

    What about Plomin’s research on genes for intelligence?

    Wade, 1998: "Dr. Plomin has sought to move the debate forward by arguing that if genes for intelligence exist it should be possible to track some of them down through the powerful new genetic scanning techniques that have recently become available. Searching through a small part of the human genome, the long arm of chromosome 6, he found that a particular variant of a certain gene was twice as common in his sample of children with ultra-high IQs than in those with average IQs. The gene has a very small effect, accounting for about 2 percent of the variance, or 4 IQ points, Dr. Plomin said."

    "So slight an effect would be expected in a trait influenced by many genes. There might be 50 or more genes affecting intelligence, experts say, and a person with a high IQ would have the favorable versions of only some of these genes. Only half the children with high IQ’s in Dr. Plomin’s study had the intelligence-promoting form of the gene he detected."

    "The research, led by Robert Plomin of the Institute of Psychiatry in London, identified six genes that were strongly associated with high or low intelligence, but even the most powerful of these accounted for just 0.4 per cent of the variation in intelligence between individuals. The six together accounted for about 1 per cent of the variation in intelligence."

    Genes will not be all that matter. What about Lewontin’s reaction norms?

    In December of 2009, James Watson expected the cost to sequence an individual’s genome would fall to $1,000 in three years time. Three and a half years ago, he thought key genes for human intelligence might be found in ten to fifteen years.

    Sharon Begley: Adding the newly discovered genes "did not improve the ability of a model that included age, sex, and apoE to predict" whether someone would develop Alzheimer’s. The genes, concluded the scientists, were "not clinically useful."

    In a phone interview, Breteler went further. "Adding these genes to traditional risk factors, such as age and sex, does nothing to aid prediction" of whether someone will develop Alzheimer’s, she told me. "Knowing your genetic status will not help. We may still be in the Stone Age when it comes to gene-based prediction."

    It seems the case for genes for behavior is weak. Still I wonder what Watson and Plomin are doing these days with their "powerful new genetic scanning techniques".

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  5. 5. FOOZLER8 9:34 am 05/4/2011

    It’s only the case that single genes for behavior are elusive. I believe that everything is genetic in part and the Big Five personality traits prove that to a certain extent – half or more of all of them are genetic.

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  6. 6. marywaye 7:02 am 05/5/2011

    How about these suicide susceptibility gene studies (just to name a few):
    1. The recent report about haplotypes in FKBP5 gene that are associated with completed suicide. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Jan 15;35(1):252-6. Epub 2010 Nov 26.

    2. Association of 14-3-3 gene haplotype with completed suicide in Japanese published earlier in Journal of Human Genetics (2005) 50, 210-216; doi:10.1007/s10038-005-0241-0

    3. Association of RGS2 Gene Polymorphisms with Suicide and Increased RGS2 Immunoreactivity in the Postmortem Brain of Suicide Victims
    Neuropsychopharmacology (2008) 33, 1537-1544; doi:10.1038/sj.npp.1301557; published online 29 August 2007

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  7. 7. joe poppa 11:09 am 05/5/2011

    I was told a joke, recently, that seems fitting, here. A scientist was observing a trained flea and said, "Jump, flea, jump." The flea jumped. Said scientist then proceeded to remove a leg from the flea, after which said scientist said,"Jump, flea, jump." The flea jumped. Said scientist then repeated the procedure until all but one leg was gone and the flea jumped, each time. Said scientist then removed the last leg and said, "Jump, flea, jump." The flea only looked up with no other response, and said scientist wrote in his journal, "After removing all legs, the flea became deaf." The Association Game is a dangerous business, and how the term starts is a clue to its consequences. Felix Unger would be more than happy to tell you all about how that goes. It is only when someone can lead me by the hand down the garden path that I will believe what I hear. One thing I’ve learned, by the way, is never believe any medical information given through the boob tube. TV is all about ratings, and they could care less about the accuracy of the information they give. One more thing: nutrients have at least an equal footing with anything else when it comes to behavior. Receptors are highly absorptive when the body is low on a nutrient, and I have never had a better orgasm than when I suddenly took Arg (it was an out-of-body experience), have never had a more vivid hallucination than when I suddenly took Glu. Well, there was the one time I’d been driving for forty hours, and I saw a giant squirrel growling and hissing at me from the back of a semi.

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  8. 8. jessc217 7:35 pm 06/19/2012

    More and more behavior studies found that there is a connection between our genes and our behavior. After reading the research article on the study of the mice’s aggression behavior by Dayu Lin (2011) in Nature, I do believe that there is a connection between genes and behaviors. However, the human body is a very complex system. An action is usually carried out by more than one gene, or is backed up by other systems when a mistake or error occurs. Furthermore, the more important that the action of a gene carries out, the more extra genes are existed in our genomic to recover that action. Even if there is a connection between the CMYA5 gene and a person’s risk of developing schizophrenia, there are still a myriad of factors that may contributes to a person’s risk for developing schizophrenia. A person with a family history of schizophrenia is considered to have a higher risk of developing schizophrenia himself or herself, and this is thought to be caused by their genes. However, families usually experience a similar environment, and people have been saying that the environment also affects one’s behavior. Therefore, I am wondering if the environment, rather than the gene, contributes to the development of schizophrenia. If so, which of these two factors, genes or the environment, have the bigger influence on the development of schizophrenia or one’s behavior?

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