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A Moral Gene?

The views expressed are those of the author and are not necessarily those of Scientific American.

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If our moral psychology is a Darwinian adaptation, what does that say about human nature? About social policy, which always presupposes something about human nature? About morality itself?
- Steven Pinker

Morality is often considered to be the domain of philosophers, not biologists. But scientists have often wondered what role our genomes play in directing our moral compass. Today, a paper was published in the open access journal PLoS ONE which found moral decision making was influenced by different forms of a single gene.

Picture yourself standing at branching train tracks with a unstoppable train barreling towards you. On one side, an evil villain has tied five people, while on the other, he has tied only one. You’ve got the switch in your hands which chooses which track the train goes down. Do you feel it’s morally acceptable to choose to kill the one instead of the five?

The scenario above is an example of foreseen harm. When such harm is unintentional, like in the train situation, most people are willing to go with Spock and say that the needs of the many outweigh the needs of the few. But previous research has found that people taking a particular group of antidepressants called selective serotonin reuptake inhibitors (SSRIs) were different – overall, they were less willing to say that killing the one person is morally justified, even if it’s unavoidable.

Serotonin is a chemical released at the junctions between nerves as a part of signaling in the brain. Since lower levels of serotonin are linked to sadness and depression, it is thought that by preventing the reuptake of serotonin, SSRIs fake higher overall serotonin levels and thus boost happy feelings.

But the connection between SSRIs and morality got Abigail Marsh and her colleagues from Georgetown University and the National Institutes of Health thinking. They knew that natural variation in serotonin reuptake ability exists in the population because of alterations in the promoter for one of the serotonin transmitter genes. People with the long form of the promoter (L) have normal levels of reuptake, while those with a truncated version (S) have reduced serotonin reuptake, similar to taking an SSRI. The researchers wondered if this natural variation influenced moral decision making in the same way that treatment with an SSRI does.

So, they took 65 healthy volunteers and tested their genes to see what versions of the promotor they had. Overall, 22 had two copies of the long form of the gene (LL), 30 had one of each (SL), and 13 had two copies of the short form of the gene (SS). They then asked these individuals to rate the overall morality of a variety of scenarios, including ones like the one above where one person is unintentionally harmed to save five others.

The results were clear: although the three groups showed no differences when presented with morally neutral scenarios or those where harm is intentionally caused to an individual, there were significant differences between groups when it came to scenarios of foreseen harm. Those with the long form of the promoter were much more willing to approve of harming one person to protect five. They felt that doing so was the better moral choice:

Those with the short form of the gene, however, felt that harming the one was morally neutral.

“I think this study is useful in helping to point out that maybe the way people arrive at their moral intuitions is just different for different people, in ways that are very deeply rooted,” says Marsh, the lead author, in a press release. Indeed, moral decision making may be as deeply rooted as it can be – that is, in our genomes.

Of course, as the quote from Steven Pinker at the beginning alluded, this kind of result leads to bigger questions. How has natural selection shaped what we think is right and wrong? How much of our moral code is influenced by our genes? And what does this say about the nature of morality itself?

Research: Marsh, A., Crowe, S., Yu, H., Gorodetsky, E., Goldman, D., & Blair, R. (2011). Serotonin Transporter Genotype (5-HTTLPR) Predicts Utilitarian Moral Judgments PLoS ONE, 6 (10) DOI: 10.1371/journal.pone.0025148

Christie Wilcox About the Author: Christie Wilcox is a science writer and blogger who moonlights as a PhD student in Cell and Molecular Biology at the University of Hawaii. Follow on Google+. Follow on Twitter @NerdyChristie.

The views expressed are those of the author and are not necessarily those of Scientific American.

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  1. 1. dnixon 9:14 am 10/6/2011

    I am disappointed that Christine Wilcox felt it necessary to refer with approval to a false hypothesis in her post.

    She wrote: “Since lower levels of serotonin are linked to sadness and depression, it is thought that by preventing the reuptake of serotonin, SSRIs fake higher overall serotonin levels and thus boost happy feelings.”

    Note the use of passive voice, “it is thought”. Does the author believe it? She doesn’t say. She just pitches it in to her essay, as if it were a necessary premise. It is not clear why she feels it is necessary.

    However that may be, the claim about serotonin (quoted above) is known as the monoamine hypothesis or the chemical imbalance theory of depression. This theory is false and has been known to be false since 1974 when serotonin levels were shown to be identical in populations of depressed and normal people.( )

    Even the FDA admits as much: “‘Biological psychiatrists have looked very closely for a serotonin imbalance or dysfunction in patients with depression or obsessive compulsive disorder and, to date, it has been elusive,’ says Dr. Wayne Goodman, Chair of the US Food and Drug Administration (FDA) Psychopharmacologic Drugs Advisory Committee. Although an SSRI may work well in an individual, this ‘doesn’t prove that there is an underlying imbalance, defect or dysfunction in the person’s serotonin system,’ he added.” (Colin Meek, “SSRI ads questioned” CMAJ. 2006 March 14; 174(6): 754.)

    This is not a secret. Well known researchers and psychiatrists have been saying this for years. Here is a sample:

    1. “The serotonin theory of depression is comparable to the masturbatory theory of insanity.” David Healy, psychiatrist.

    2. “A serotonin deficiency for depression has not been found” Joseph Glenmullen , Harvard Medical School.

    3. “Indeed, no abnormality of serotonin in depression has ever been demonstrated” David Healy, Psychiatrist.

    4. “We have hunted for big simple neurochemical explanations for psychiatric disorders and have not found them.” Kenneth Kendler, Psychiatrist.

    5. “there is no clear and convincing evidence that monoamine [e.g., serotonin] deficiency accounts for depression” Stephen M. Stahl, Psychiatrist

    These views are cited by Lecasse and Leo in their 2005 article, “Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature”

    I leave it to the author to declare whether she thinks the monoamine hypothesis is critical to the research she discusses. But the wide popular acceptance of the folklore about this hypothesis has more to do with the advertising budgets of the pharmaceutical companies than the scientific evidence. It is too bad that she seems unable to tell the difference.

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  2. 2. all4kindness2all 7:39 pm 10/6/2011

    I am always dismayed by science trying to leap to conclusions like these from so little evidence.

    While I think the idea that our genetic make-up influences who we are is a valid one, it seems a bit soon to jump to specific genes when we don’t understand or treat depression successfully.

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  3. 3. Vitis01 11:29 pm 10/6/2011


    “I leave it to the author to declare whether she thinks the monoamine hypothesis is critical to the research she discusses.”

    Or you could just follow the link at the bottom of the article.
    In the time it took you to write that incredibly condescending post you could have read the three short paragraphs that summarize the research and answered the question yourself.

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  4. 4. dnixon 5:21 am 10/7/2011


    Implicit in your comment is that it is unreasonable to expect that the post by Christie Wilcox should be able to stand on its own merits. I reject this idea and, for that matter, I wouldn’t be surprised if she did too.

    You say my comment is condescending but do not take issue with my argument, condescending or not.

    It is not condescending to call for a stop to the gratuitous insertion of patently false folkloric notions, e.g., the monoamine hypothesis, into an essay about the brain, its neurotransmitters and their genetic ground. It is simply a call to observe the limits of what the evidence warrants. This is a modest expectation and hardly condescending. I do confess to impatience with the continuing practice of citing the hypothesis as if it were anything other than junk science.

    I’ll take this opportunity to apologize to Christie Wilcox for getting her name wrong in my first post where I called her Christine.

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  5. 5. Vitis01 6:42 pm 10/7/2011

    It is possible for an argument to be reasonable while the method by which that argument is delivered is still over-the-top and condescending. I think it is usually bad form to refer to a blog author in the third person on her own blog. It is not your place to lecture her in her own classroom (so to speak). Ask a question to start a discussion. I feel that that is both more interesting and less presumptuous.

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  6. 6. John W. Bales 9:40 am 10/8/2011

    Morality provides guidance in living successful lives long-range. It does not preordain proper split-second decisions in life-or-death emergencies. Speculation about how one would respond in such a situation is exactly that–speculation. It is highly doubtful that it indicates the respondent’s moral values.

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  7. 7. Rosita 2:33 pm 10/9/2011

    dnixon and all4kindness2all:

    1. There is obviously disagreement among neuro-scientists on the theory that you claim was irrevocably disproved many years ago. The research which Wilcox summarizes appears to base its hypothesis on some version of this theory. Wilcox is not responsible for presumably informed beliefs of these researchers. Unless you can prove that Wilcox inaccurately reported the theoretical basis of this research you should castigate the researchers for their “error”, not resort to fallacious ad hominem attacks on Wilcox for summarizing it.

    2. The validity of the argument that Wilcox is making on behalf of the moral researchers is not dependent on whether aberrant serotonin levels are directly responsible for clinical depression, are the result of clinical depression or are involved only because the system that causes them is implicated in clinical depression.

    The essential point of this research is that genes that affect how a brain chemical is manufactured or utilized has been shown to affect how people decide what is moral and what is not. It does not matter at all whether these genes, or their expression, have any effect on mood or mental illness. Your point is a complete “red herring”.

    John Bales:
    The point is that genetic makeup affects how a person processes moral reasoning. It does not matter whether this only affects “split second” reasoning or whether it affects carefully considered moral reasoning. It does not matter whether or not the decisions these people make in the split-second hypothetical experimental condition would be exactly equivalent to the actions the person takes in real life. The point, to repeat it, is that the experiment provides intriguing support for the notion that what a person considers “moral” is influenced by their innate genetic make-up and is not entirely dependent on socializing influences, including the dogmatic teachings of whatever religious viewpoints they have been exposed to in their formative years.

    It is already well known (even to you)that equally devout adherents to the same religion, and even the same brand of religion, come to opposing beliefs about what is “moral” and what is “immoral”. If this were not the case then all equally devout religious believers would be in complete agreement about what is “evil” and what is “good”. There would be no need for apologists to spend time engaging in semantic tap dancing in order to reconcile the barbaric acts, commandments, encouragements and entrapments of the ancient Jewish war god vis a vis the modern moral memes that are supported by those most concerned with supporting and expanding human rights and dignities.

    The underlying implications of the research that Wilcox summarizes is that people are deeply deluded if they imagine that they can determine what is “universally” or “absolutely” moral, or what some version of god thinks is “moral” merely by reference to their “gut feeling” about it or their mind-biased interpretation of some holy writings.

    There is ample evidence that the brain is easily deluded, easily influenced by environmental input and easily blinded by socializing background. Now there is evidence that some the biases that fuel these delusions are inbuilt. It is no secret among moral researchers and behavioral scientists that the “morality of god” is always equal to the perceived morality of the particular religious adherent.

    In other words, this is quite a blow to the religious notion of “absolute” morality and the notion that every person is equally capable of coming to the “right” conclusions about what is moral.

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  8. 8. dnixon 10:48 pm 10/9/2011


    You say that I “resort to fallacious ad hominem attacks on Wilcox”. I suggest you don’t know what an ad hominem attack is. Did I suggest that her argument is false because of who she is or what she does for a living? No. I am critical of her essay because of what she wrote, not because of who she is.

    Indeed, the meaning of words seems to escape you elsewhere in the brief compass of your remarks. I said and affirm now that the monoamine hypothesis was disproved in 1974 and cited the study that did it. For you, however, it appears not to be enough to disprove a theory once. You seem incredulous that I should imagine it to have been “irrevocably disproved.” Do you think there is some epistemological safe haven where disproved theories may hang out so that they can pop up again, made new and whole, to contend again for our allegiance? Surely not. A disproved theory is just that and it is disproved for all time. It matters not a whit whether it was disproved “many years ago” or yesterday. And since, in science, the truth is not determined by vote, you can line up all the neuro-scientists in the world who think otherwise and it just doesn’t matter. Does it?

    But of course I didn’t leave it with the lone citation of the 1974 Bowers study. I cited the person in the FDA most responsible for keeping track of the work of what he calls “biological psychiatrists”. He admits that the necessary evidence upon which the monoamine hypothesis hangs is lacking. I cited the judgment of researchers and practitioners, well known in the field who also deny that it has an evidentiary basis.

    I thought that would be enough. But no. Yet, neither you nor the other defender of the essay cite anything. You merely scold. Well, that just won’t do.

    Had I wanted to write a longer comment, I could have reviewed the history of the hypothesis showing that it was developed before double blind, randomized studies were invented; that it was based in part on a manifestly incorrect view of what effect reserpine had on mood. I could have described what Irving Kirsch refers to as the nail in the coffin of the hypothesis; that selective serotonin reuptake ENHANCERS work about as well on the symptoms of depression as SSRIs.

    In spite of all the evidence, the folkloric nonsense of the monoamine hypothesis is trotted out by people who ought to know better to fill in pesky gaps in an unfolding argument or presentation. And with every such usage, whether it be the keystone or an incidental appendage to an argument, the unsuspecting will be encouraged to believe it. People are still being told that they have an imbalance in their brain chemistry and this drug (take your pick of SSRIs, TCAs, MAOIs) will correct this imbalance. This, in spite of mounting evidence of the harmful side effects of these compounds, including risk of suicide, obesity and diabetes, serotonin syndrome, loss of libido, and, as Giovanni Fava has long argued, permanent imbalance of brain chemistry and increased resistance to medication and likelihood of relapse.

    So, instead of using the intellectually lazy phrases like “appears to” and “presumably informed”, take responsibility and stop with the excuses. Either show credible evidence for this hypothesis or stop mentioning it.

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