Psychopathic Empathy

Introductory waffle

This week’s blog post is a little different. In part, it is a response to my students’ requests for a demonstration of the “critical thinking” I keep demanding from them. Fair enough. It is important for people to be as clear as possible about what they mean when they use ‘technical’ words and phrases. Accordingly, this post provides a partial critique of a recent paper relevant to this week on my altruism module. That paper, by Meffert et al. (2013), has been widely reported as showing that:

An 'empathy switch' allows psychopaths to feel at will

The central claim

Meffert and her colleagues claim to demonstrate a need for “a profound reconceptualization of psychopathy” (p. 2559). They note that psychopaths are usually portrayed as having “a profound lack of empathy” (p. 2550) due to their deficient brains making them incapable of caring about others’ welfare. Against this, Meffert et al. (2013) claim to show that, while psychopaths usually don’t care about others’ welfare, they can do so when motivated to try.

See how I can force myself to share your joy at this stunning news!

The evidence

There are two main parts to Meffert et al.’s evidence.

The first they claim shows that, as commonly believed, non-psychopaths typically have more pronounced reactions to others’ experiences than do psychopaths. The second they claim shows that psychopaths and non-psychopaths have (more) similar reactions to others’ experiences when each is deliberately trying to empathise.

The samples

For key similarities and differences across groups to be meaningfully interpreted it is important to know how comparable the groups are. Meffert et al.’s paper does not make it easy to determine such things.

Almost nothing is said about who the control group were (e.g., members of the general public) or about how either the control group or the psychopathic (“target”) group were recruited.

In the “Participants” section on p. 2551, the paper says that the control participants were male and had the same handedness as members the target sample. (Many neuroimaging studies exclude left-handed people.) It also says that the target group and the control group had, on average, the same age and IQ. I could not find a report of how low or high that average IQ was.

Later in the paper, Meffert et al. reveal that the control group also differed from the target group on a range of “factors linked to criminal lifestyle (e.g., lower level of education, history of drug abuse and length of incarceration)” (p. 2558).

Given this, attributing found differences between the target and the control groups specifically to their differences in psychopathy levels seems somewhat bold, especially if they could plausibly stem from other differences between the groups.

Generalisability

As just seen, the term “psychopaths” does not capture all that was distinctive about Meffert’s target sample. As well as being diagnosed as psychopathic, the eighteen members of that sample were also Dutch, adult, male, poorly educated, right-handed, incarcerated criminals, the vast majority of whom had a recognised dependence on drugs. It seems at best questionable that this tiny and highly distinct sample is strongly representative of all people high in psychopathy. Even most media headlines reporting the study took care to be clear that the findings relate most obviously to criminal psychopaths.

Of course, if the study compellingly shows that any psychopaths (perhaps especially criminal ones) can care about others’ welfare (perhaps especially that of anonymous strangers), that may indeed suggest that a profound reconceptualization of psychopathy is needed.

Confirmation of a psychopathy difference across samples

To attribute other differences between the two groups to their difference in psychopathy, one clearly needs to be pretty sure that there are differences in psychopathy across groups. In Meffert et al.’s study members of the target sample were all diagnosed as psychopaths and members of the control group (as far as I can tell) were not. Nevertheless, it makes sense to check and Meffert et al. did. All participants completed a 187-item self-report measure of psychopathy (p. 2551).

As expected, the control group obtained a lower average score on this Psychopathic Personality Inventory (PPI) than did the target group: about 399 vs. 422 (Table 1, p. 2555), a statistically significant difference (p < .05, p. 2554).

If I had more time I would examine this result a lot more closely. Like many psychiatric diagnoses, “psychopathy” is somewhat an umbrella condition and two people or samples with identical scores might obtain those scores because of very different qualities. Moreover, Meffert’s control group psychoticism score of 399 is much higher than the average score of 268 obtained by some very scary criminals sampled in a study by Copestake et al. (2011).

                                                                                                  

For the sake of argument, though, let’s accept that Meffert et al.’s target group members were psychopaths (among other things) and that their control group members were not.

The “spontaneous empathy” task

All participants watched short video clips of two hands interacting. The hands interacted in several ways, two of which are more important than the others. In the “love” interactions an “approaching” hand stroked the back of someone else’s “receiving” hand, which gave a tender squeeze in response. In the “pain” interactions the approaching hand pulled back one of the receiving hand’s fingers to a point that would be painful for most people.

Participants in this spontaneous empathy task were given the rather strange instruction to view the film clips “as if they were watching one of their favourite videos” (p. 2552). Call me strange but I’d find it quite unsettling pretending that my favourite videos comprised largely of clips in which people were inexplicably deliberately hurting others!

Initial results

The two groups had differing brain activation in “a large network of regions” (p. 2555). In each of these regions the control group showed higher brain activation than did the psychopath group (Table 2 and Supplementary eTable 2). Some of these Meffert et al. considered regions of particular interest because past research suggests that they are sometimes similarly activated both by personal experience and by observation of others having similar experiences (p. 2553). These included “the dorsal and ventral premotor cortex, primary and secondary somatosensory cortices, the anterior insula and the cingulate cortex” (p. 2555).

Accepting for the sake of argument that these findings and the authors’ interpretations of them are valid, “individuals with psychopathy showed … reduced activation” compared to control participants in brain areas associated with (among other things) vicarious experience, sensations, and emotions (p. 2558).

To report these results slightly differently, when instructed to watch short clips of interacting hands as if they were watching their favourite videos, poorly educated, incarcerated, drug-dependent, male criminals with relatively high levels of psychopathy appeared not to react as emotionally as did relatively well-educated, non-addicted, non-criminals with relatively low levels of psychopathy.

Maybe this indicates a difference in spontaneous empathy and maybe it results from a difference in levels of psychopathy across groups. Many other possibilities seem at least plausible.

My guess is that members of the target group were less motivated and anyway less able to comply with the task. I also doubt that this was primarily due to differences in psychopathy.

It seems at least possible that the control group members were more or less willing and able to comply with the instructions and they accordingly became relatively engrossed in the task of trying to conceive of the emotionally-evocative hand-theatre as high-drama. I suspect that the uneducated, drug-addled, career criminals would have really struggled (if they even tried) to successfully enter into the same spirit. If so, the brain activation differences across groups stemmed from the different engagement in the task due to different compliance with the viewing instructions, which itself stemmed mainly from the factors that happened in this study to be associated with psychopathy.

This is of course only my guess. The much more important point is that there is no compelling evidence which enables anyone to choose between my guess and Meffert et al.’s interpretation of their findings. The first part of their study may or may not tell us anything about psychopathy and if it does, there is no telling what, exactly. The two groups differed on too many potentially important characteristics, the instructions given to participants before the main task plausibly promoted different responses in each group, and no checks were made for differences between the groups in such things as task-engagement (e.g., how much participants tried and succeeded in viewing the clips as though they were their favourite movies), task-accuracy (i.e., how well each group recognised the emotional content of the viewed videos), subjective experience during the task (e.g., how emotionally aroused participants felt and what specific emotions were involved), or how they felt “on behalf of” the hands/people in the video clips (e.g., "empathic" joy, distress, anger, etc.).

In some ways, perhaps it doesn’t matter. In this part of the study, Meffert et al. are pushing at an open door. As they note themselves, the claim that psychopaths empathise less with others’ experiences than do non-psychopaths is the standard view – as well it might be because having a lack of empathy is part of the diagnosis for being a psychopath!

Let us therefore move on the second strand of evidence considered by Meffert et al.

The “deliberate empathy” task

Participants next watched a slightly different series of hand-interaction video clips, some showing nothing but “loving” interactions and some showing nothing but “painful” interactions. This time, participants received instructions to “feel with” one or other of the hands.

In this task, there were still many differences in brain activation across the groups (Supplementary eTable 3) but (a) it varied which group had the higher level of activation in a given area, (b) almost none of the areas of differential activation occurred within the researchers’ identified regions of interest (Table 3), and (c) there was less difference in brain activity between the target and control groups than had been the case in the “spontaneous empathy” condition.

Thus, in brain areas relevant to having similar experiences to those others seem to be having, psychopaths were not that different to non-psychopaths during this “deliberate empathy” task. The authors conclude that psychopaths are almost as able to experience vicarious emotions as non-psychopaths when each is “following instructions to empathize”.

Let’s phrase this conclusion a little more conservatively. If valid, this part of Meffert et al.’s study finds relatively little difference in brain activation when (druggy, criminal, etc.) psychopaths and (non-druggy, non-criminal, etc.) non-psychopaths are instructed to “feel with” someone else’s hand which is giving or receiving either a loving caress or a painful smack with a ruler.

Meffert et al. provide one possible explanation for this, i.e., that all participants were feeling love or pain as though they were actually experiencing caresses or smacks themselves. Another possibility is that no one was feeling very much, in either group. No measure was used to check this either way.

Being asked to “feel with” a hand that one is watching on a video is an odd instruction. Imagine being a participant in this study yourself. If you were told to “feel with” a videoed hand hitting someone else’s hand with a ruler, do you imagine that it would feel like your hand was swooshing down and reverberating with the shock of contact? Or do you imagine that you would try to work out what sorts of experiences an owner of such a hand might be having, perhaps by imagining how you might feel in such a situation? If like me you find the ‘working out’ possibility plausible, it seems at least possible that both groups were engaging in quite a lot of thinking about others’ feelings – without necessarily having comparable (“vicarious”) feelings themselves.

Such a possibility may seem particularly credible when we learn that during this task the target group had relatively high activity in “mentalising” areas of the brain, i.e., those thought to be involved when trying to work out what others are experiencing (p. 2559). It is widely acknowledged that psychopaths can be good at identifying others’emotions, all the better to exploit them for personal gain.

As in the first part of the study, Meffert et al. do too little to work out what participants in each condition are doing and experiencing to be confident about how best to interpret the differences in the brain activation they find – still less the differences they don’t find.

Conclusion

The most important of Meffert et al.’s findings for their key claim is that uneducated, criminal, drug-addicted psychopaths and educated, non-criminal, non-addicted, non-psychopaths show relatively similar levels of activation in brain regions associated with vicarious emotions when instructed to “feel with” one or other hand in short videos of hands interacting in apparently loving or painful ways.

One possible reason for this is that the uneducated, criminal, addicted psychopaths had subjective experiences that corresponded in some way to those portrayed in the videos (to about the same extent that anyone else would) and one possible and scientifically dramatic implication of this is that psychopaths can care about the welfare of others when they choose to do so.

Another possibility is that, regardless of levels of psychopathy, all participants in this part of the study were trying to work out what experiences others might be having and this did not markedly involve anyone actually having “vicarious” feelings (or being concerned about the welfare of anyone else having similar feelings). This possibility would do nothing whatsoever to threaten standard conceptions of psychopathy.

Given the multiple impediments to confidently interpreting Meffert et al.’s results, much more and much better evidence is needed before there is good reason to suppose that psychopaths are able to share or truly care about others’ emotional experiences. 

Caveats

Meffert et al. (2013) is much more complicated than I have let on here. I am not a neuropsychologist and I am not familiar with many of the methodological and statistical procedures reported in Meffert (2013). This means that you should be particularly sceptical of any of my claims above which might be hindered by these inadequacies on my part. On the other hand, there are problems with the paper that, because of time and presentation issues, I did not make explicit here (e.g., the potentially rather suspect practice of comparing brain activation in the “spontaneous” and the “deliberate” empathy parts of the study) and there may be other – perhaps more serious – problems with the paper that I am simply not skilled enough to notice. If anyone would like to correct my claims or make new ones in the comments section below, your contribution to my and my students’ education will be most welcome.

References and further reading

Chambers, C. (2013, Nov 25). Could a brain scan diagnose you as a psychopath? The Guardian [Link]

Copestake, S., Gray, N. S., & Snowden, R. J. (2011). A comparison of a self-report measure of psychopathy with the psychopathy checklist-revised in a UK sample of offenders. Journal of Forensic Psychiatry & Psychology 22(2): 169–182.

Jarrett, C. (2013, Dec 13). A calm look at the most hyped concept in neuroscience – Mirror neurons. Wired. [Link]

Jarrett, C. (2012, Dec 10). Mirror neurons: The most hyped concept in neuroscience? Psychology Today [Link]

Lamm, C., & Majdandžić, J. (2014). The role of shared neural activations, mirror neurons, and morality in empathy-a critical comment. Neuroscience Research. [Link]

Neuroskeptic (2014, July 21). Functional neuroimaging’s Neymar problem. Discover. [Link]

Neuroskeptic (2014, June 6). fMRI motion correction: The quick and the dead. Discover.  [Link]

Neuroskeptic (2013, May 13). Looking Askance At Cognitive Neuroscience. Discover. [Link]

Neuroskeptic (2013, April 27). The (sigh) psychopath brain. Discover. [Link]

Neuroskeptic (2012, April 25). Does brain scanning show just the tip of the iceberg? Discover. [Link]

Neuroskeptic (2009, Sept 16). fMRI gets slap in the face with a dead fish. Discover. [Link]

Vincent, J. (2013, July 26). An 'empathy switch' allows psychopaths to feel at will. Discover. The Independent. [Link]

Wikihow. How to identify a psychopath. [Link]

Picture credits

Psychotic empathy doll [Link]

Forced smile [Link]

Sherlock Holmes [Link]

Snakes in suits [Link]

How to cite this blog post using APA Style

See: http://owl.english.purdue.edu/owl/resource/560/10/

T. Farsides. (2014, November 17). Psychopathic empathy. Retrieved from http://tomfarsides.blogspot.com/2014/11/psychopathic-empathy.html 

Empathy

Introductory waffle

This is very much a work-in-progress blog post, written in a bit of a rush. I hope to edit it ‘sometime’ to make it more clear, readable, and engaging, especially for non psychology students. This blog post spans content covered in two consecutive weeks of my altruism module: “Mind-reading and morality” and “Passion and emotion”.

“Mind-reading and morality” considers the role of understanding in caring about the positive welfare of others (called “altruism” on the module and in this blog). Such understanding has two (or three) components: understanding others’ specific experiences or situations and understanding others-as-individuals-worthy-of-concern.

“Passion and emotion” considers the role of emotions in caring about the positive welfare of others; both as potential causes of altruism (e.g., guilt, gratitude, etc.) and as potential manifestations of altruism (e.g., pity, sympathy, compassion, etc.).

Many of these topics will merit its own blog post in time, fate willing. In this one I focus on yet another term that is routinely used in a way that impedes rather than promotes understanding and progress: “empathy”.

What is empathy?

Adopting my now-standard practice of trying to delineate distinct phenomena rather than make claims about what empathy “is” or “really means”, here is a list of what might be argued to be its main aspects, building blocks, or types:

1.      Other-understanding, i.e., having beliefs about another’s experience or situation.  These can vary in how accurate they are (a.k.a. “empathic accuracy”). 1b. The processes used in reaching other-understanding are often also referred to as aspects of “empathy” but are probably better referred to as methods of attempted mind-reading.

2.      Contagion, i.e., having experiences that are triggered by and similar to another’s experience. Most commonly this is discussed in terms of “sharing” another’s emotional experience, e.g., being distressed because another is distressed (a.k.a. “empathic distress”) or joyful because they are joyful (a.k.a. “empathic joy”).

3.      Consideration, i.e., behaving in ways that suggest concern for another’s positive welfare; “showing” or “demonstrating” empathy. From my point of view, a manifestation of altruism.

Because these seem to be distinguishable phenomena, it would seem wise to call them different things. This is true even if they are related. Indeed, it is especially true because they are sometimes related. If we want to understand the causes, correlates, and consequences of each of these things, and the relationships among them, it really cannot help to use the term “empathy” willy-nilly for each or any of them.

Potential determinants of empathy

By which I mean things that may sometimes lead to one or more of: other-understanding, contagion, or consideration. Confusingly, if unsurprisingly, each of these potential determinants is also regularly if erratically referred to using the term “empathy”. For example:

Perspective-taking, i.e., trying to imagine what another person is experiencing, what one would be experiencing were one in another’s situation, or both. Perspective-taking can be fostered by other processes that are themselves sometimes called “empathy”, e.g., identification (feeling an association or affiliation with another because of perceived or fantasized similarity).

Mimicking, i.e., copying something about someone else, e.g., their posture.

Projecting, i.e., the act of imputing characteristics to others rather than genuinely perceiving such characteristics in them. This may result from expectations, desires, or both.  Having “put them there”, it is easy for people to then reach beliefs that they are there.

Attention to another, e.g., their expressions, posture, self-reports, etc.

Again, understanding the unique and common causes, correlates, and consequences of other-understanding, contagion, and consideration is unlikely to be helped by promiscuously and indiscriminately calling all three of them and potential determinants of one or more of them “empathy”.

When the title or abstract of a scientific article reports some discovery concerning “empathy”, I genuinely have only a hazy and tentative notion of what that article is likely to be about. It might be about almost anything between a dispositional tendency to be concerned about the positive welfare of others (i.e., trait altruism) to an ability to spot which of four facial expressions is registering disgust (i.e., accurate emotion recognition). That can’t make for good science.

Empathy in the Empathy Altruism Hypothesis

The longer I teach about the Empathy Altruism Hypothesis (EAH), the more I am reminded of the witticism that the Holy Roman Empire was not holy, Roman, or an empire.

I have previously suggested that the “altruism” discussed in the EAH (i.e., a qualitatively distinct form of motivation in which pursuit of personal goals plays no essential part) is a chimera. Nevertheless, “empathy” as discussed in the EAH does sometimes seem to promote altruistic helping as the term is used here, i.e. helping motivated by concern for the positive welfare of another.

It therefore becomes important to be clear about what sort of empathy that is. Again, I have discussed this previously. To recap, it is the experience of a set of emotions: compassion, sympathy, tenderness, warmth, softheartedness, and feeling moved. Batson notes that others prefer to label this collection of emotions with one of the emotions within the collection, e.g., compassion or sympathy. I am one of those others.

So, the EAH predicts that when we feel compassionate or sympathetic towards others  we will sometimes try to help them.⁽¹⁾ I have absolutely no issue with this. Surely only someone confused by jargon could possibly object!

This does not mean that that any alleged type of empathy promotes altruism. Only that compassionate emotions can. If you want to claim that some other alleged type of empathy also promotes altruism, you need to provide some evidence about that specific relationship. (Some of the EAH literature will help justify some such claims, e.g., claims about links between other-understanding and sympathy.)

(1) Mainly when our help seems necessary and sufficient to improve their welfare and we are not overwhelmed by contrary concerns.

Other-understanding and consideration don’t entail contagion

(Alternative sub-title: Empathy is not necessarily empathic)

It seems possible to understand something about others’ situations and strive to make things to be better for them without sharing their feelings. Surgeons can understand that anesthetised patients they care about will benefit tremendously from a well-executed operation and therefore be motivated to be as effective as possible in helping them. Their other-understanding and consideration seem unlikely to result from or even to be accompanied by them “catching” their patients’ feelings. Hopefully, their patients temporarily have no feelings at all!

Similarly, and to reiterate a point I have made in an earlier post, humans can feel compassion and concern for people who are currently quite happy (because we know and they do not that they are in peril) and for wholly imaginary entities (e.g., fictional characters, cartoon characters, characters represented by video game avatars, etc.).

So, whatever alleged empathy you may be considering, if you want to make claims that it is the result of emotional contagion or similar, please provide evidence beyond “It’s empathy, in’it?” This includes claims about empathy in the EAH.

Against Paul Bloom

Paul Bloom has taken a public stance “Against Empathy”. He recognises that his position is “outlandish” and hastens to be clear that he is not against “morality, compassion, kindness, love…” and nor he opposed to other-understanding or to promoting others’ welfare. He is only against (certain instances of) people “experiencing the world as others [apparently] do”. Broadly, he is against emotional contagion (in some situations).

I have various complaints about Bloom’s article and associated stance. One main complaint is that Bloom repeatedly uses the term “empathy” loosely, inconsistently, and expediently. The other is that this unhelpful provocativeness is beneath Bloom. Paul Bloom is a very fine scholar, scientist, writer, and raconteur who is engaged here in a project that makes scholarship, science, and perhaps even morality harder than it would be had he not gone down and remained so committed to this path. (See also my comment below his article.) You wanted a nemesis, Professor Bloom :-)

Mirror neurons and empathy

A detailed discussion of mirror neurons will have to wait. The standard story is that when humans and some other animals witness another experiencing something, they and those they are witnessing experience something very similar. We wince if we see someone bang their thumb with a hammer. We feel a certain sadness when we see others who appear to be sad. Therefore, the story goes, we are “naturally empathic”. Contagion happens automatically and, according to some versions of the story anyway, other-understanding and consideration/ compassion/ altruism follow almost equally automatically.

If you want to tell a story a bit like this, you will do well to evaluate the evidence and don’t believe the hype. In particular, give some consideration to: findings that people unable to experience pain can recognise (but not “share”) others’ pain; the fact that Charlotte Willis taught me how horses express emotions; psychopaths seem unbothered by others’ distress; sports fans revelling in their opponents’ woes; people being insensitive to the misery portrayed in TV news programmes; how glorious Schadefruede and revenge can feel; and Jarrett (2013).

Summary

The term “empathy”, like the term “altruism, is used so promiscuously that it can impede clear thinking and scientific progress. When wondering about where empathy comes from or what results from it, one’s first question has to be, ‘What might be meant by “empathy”?’ When discussing empathy, one’s first responsibility is to be as clear as possible about what ‘aspect(s)’ of empathy you mean. The research literature is stuffed with nuggets about relationships between mind-reading, other-understanding, contagion, and altruism, but synthesising that literature will remain a challenge until some terminological norms take hold. I will nevertheless attempt to review many such relationships in later posts.

Further reading

Batson, C. D. (1990). How social an animal? The human capacity for caring. American Psychologist, 45 (3), 336-346. 

Batson, C.D. (2009). These things called empathy: Eight related but distinct phenomena. In J. Decety & W. Ickes (Eds.), The social neuroscience of empathy (pp. 3-15). Cambridge: MIT press. [link]

Decety, J., & Cowell, J. M. (2014). The complex relation between morality and empathy. Trends in Cognitive Sciences, 18(7), 337-339.

Jarrett, C. (2013, Dec 13). A calm look at the most hyped concept in neuroscience - Mirror neurons. Wired. [Link]

Kerem, E., Fishman, N., & Josselson, R. (2001). The experience of empathy in everyday relationships: Cognitive and affective elements. Journal of Social and Personal Relationships, 18, 709-729

Zaki, J., & Ochsner, K. (2012). The neuroscience of empathy: Progress, pitfalls, and promise. Nature Neuroscience, 15 (5), 675-680.

Videos

One really good: What is empathy?

One that students love but which gets my goat: The power of empathy

Picture credits

Canine empathy [Link]

Helping the handless [Link]

Nemesis [Link]

Sad smiley [Link]

How to cite this blog post using APA Style

See: http://owl.english.purdue.edu/owl/resource/560/10/

T. Farsides. (2014, November 07). Empathy. Retrieved from http://tomfarsides.blogspot.com/2014/11/empathy.html

The genetics of altruism

Introductory waffle and warnings

This is very much a work-in-progress blog post, written in a bit of a rush. I hope to edit it ‘sometime’ to make it more clear, readable, and engaging, especially for non psychology students. This week’s topic on my “Altruism and helping behaviour” module is the Biology of altruism. Ideally, I would write at least four blog posts for it: this one; one on twin, adoption, and family studies; one on evolution; and one on brain stuff. There’s no way the space-time continuum will facilitate me doing all four this year, so let’s crack on and see if I can manage at least one decent draft.

I used to think that psychology got itself into serious unnecessary muddles because of vaguely defined, inconsistently applied, ill-chosen jargon. I also used to think that biology – a proper science and everything – would not be like that. I no longer hold one of these beliefs.

Below I try to explain some basics of genetics. I have never been taught genetics and haven’t studied biology since I was 12, by which time I was already well out of my depth. Be critical and sceptical about everything I say below – and indeed everywhere. But don’t be nasty. There’s rarely a good reason to be nasty.

I’m not a Gene Genie

 

DNA

Below is a representation of some DNA. The famous “double helix” is shown on the right. The “ladder” picture on the left is more useful for current purposes.

Some DNA

The “rungs” of the ladder are called “base pairs”, mainly because they are pairs of “bases” (a.k.a. nucleotides).

Bases are chemicals and in DNA there are only 4 types. These are summarised by the first letter of each chemical: A, C, G, and T. These are represented in the diagram above in red, yellow, green, and blue, respectively. (If you see a “U” when reading about bases somewhere else then something called “RNA” is being discussed and things are probably getting more complicated than necessary for current purposes.)

Bases almost always team up with a particular complementary base. They’re kind of cute like that. A and T almost always hook up together and so do C and G. If something else happens, biologists call the process and its result an example of “mutation”. Frankly, I’m surprised they had the restraint not to call it an “abomination”.

If any section of the ladder is ripped in half lengthways and some appropriate spare material is about, it is possible to make two identical copies of the original section. Each half-rung is simply completed with its complementary base: Ts are added to As, As to Ts, Gs to Cs, and Cs to Gs. Mutation aside, this happens every time the body makes a new cell. (There are approximately 37 trillion cells in the human body, almost all of which houses its own copy of the entire body’s DNA, which itself contains 3 billion base pairs in a particular order. If that doesn’t impress you when you really think about it, you are hard to impress.)

DNA section split

The term “gene” is used rather chaotically. I will try to differentiate distinct uses of the term in the hope I don’t make the situation even worse. If I fail, please forgive me.

“Protein genes”

What I am calling “protein genes” are specific lengths of DNA half-rungs.

A “protein gene”

 

The half-rungs of a protein gene act a bit like a blueprint that is used to bring about a protein. Some sets of three adjacent bases, known as “codons” or “triplets”, provide blueprints to make specific “amino acids”. Other codons provide instructions about how to combine chains of amino acids into proteins and about how to combine proteins to make more or less everything of importance in the body (with obvious exceptions such as food and aliens). If every set of three half-rungs coded (provided a blueprint) for amino acids, a protein gene could be represented a bit like this:

 In facilitative conditions, a protein gene will result in a particular protein

The illustration above of a protein gene has a particular sequence of bases. Reading from the top down, its bases are AACCTGACT … GACCTGATT. Each protein gene ‘codes’ for a single protein but varies in how many sequenced bases it has. Human protein genes have sequences of between about 27 thousand and 2 million bases. Special triplets of bases called “stop codons” indicate that either end of a protein gene has been reached.

It takes two

Each half-rung on the DNA ladder is actually a double half-rung. (I know, but try to stay with me. This really is important.) By this I do NOT mean a base-pair of two complementary half-rungs. I mean each half-rung can be thought of as comprising two half-rungs hugging each other. If it helps, imagine gluing together two more-or-less identical ladders laid one on top of the other and then splitting the combined ‘double-thick’ ladder lengthways. Each half-rung of each double-thick half-ladder will comprise a half-rung from one of the original ladders glued side by side with the corresponding half-rung of the other ladder.

The protein gene depicted above is actually better represented by making clear that there are two parts to every half-rung, so it looks a bit like this, with each letter in the top row being connected to each corresponding letter underneath:

AACCTGACT … GACCTGATT

AACCTGACT … GACCTGATT

If this was your genetic code, one letter would correspond to the equivalent one on the half-rung you inherited from your biological mother and the other would correspond to the equivalent one on the half-rung you inherited from your biological father. For convenience, let’s pretend that all the top-row letters were inherited from your biological mother and all the corresponding bottom-row letters were inherited from your biological father. (A more accurate but difficult representation would jumble them between the top and the bottom.)

Shared genes

In the illustration I just used, all of the letters for each half-rung are identical for the bit inherited from your biological mother’s DNA and the bit inherited from your biological father’s DNA. This is mostly because your biological mother’s DNA is or was very, very, very similar to your biological father’s DNA.

When two or more living things’ DNA is very similar, those living things are often said to “share” their DNA, or have “the same” DNA. To avoid becoming disastrously confused later (when considering evolution), remember that different living things neither share nor have the same DNA as each other, although they do often have very, very similar DNA.

The most likely reason that your biological mother and your biological father each had an “A” representing their first half-rung above is because most people in the world probably have an “A” half-rung at that point in their DNA. The vast majority of people’s DNA is close to being identical to every other person’s DNA.

Estimates vary (for various reasons) but it is common to hear that well over 99% of any human’s DNA is identical to the DNA of any other human. For almost their entire genome (i.e., the whole of their DNA), all humans have the same bases in the same places.

The same is true within all species. Each living thing’s DNA is nearly identical to the DNA of every other living thing within the same species.

Similar is true across species. Compare any human, chimpanzee, bonobo, gorilla, or orang-utan with any other member of these great ape species and their DNA will be at least 93% identical. This makes sense. Lots of DNA will serve similar purposes no matter which great ape it is in, e.g., to serve as blueprints to make two legs, two arms, two eyes, etc.

Large parts of humans’ DNA are more or less identical to comparable bits of the DNA of mice and fruit flies. This makes it possible to study DNA and its effects in human-relevant ways that are much cheaper and less ethically contentious than might otherwise be the case.

“75% of our genetic make-up is the same as [that of] a pumpkin” (Link).

Statistics such as the ones above are often used to reinforce the truth that humans are animals and much more similar to non-human living things than we sometimes realise or remember.

The corollary point is of course also true: living things that have a lot of identical DNA can be enormously different to each other.

Alleles

More than 99% cent of DNA being identical across humans means that any person’s DNA differs from another person’s by considerably less than 1%.

The bit of DNA that varies across humans is referred to as “polymorphic”, meaning it can take more than one form. Reiterating a point made just above, tiny DNA differences across people can have enormous effects on their bodies and therefore often their behaviour.

When differences in DNA sequences across people affect the form or function of their protein genes, people are often said to be “genetically different” from each other.  This can be confusing. A better phrase would be to say that people in this situation have different types or alleles of the same gene (which results from differences in the specific patterning of the DNA sequencing within the gene in question).

Differences across humans in a single half-rung of DNA can have important consequences. When 1% of humans or more have been found to have importantly different half-rungs, those half-rungs are said to cause (or be) “Single Nucleotide Polymorphisms”: “SNPs” or “SNiPs”, pronounced “snips”.

Here is a representation of four people’s DNA sequence for a protein gene that has alleles (different versions) resulting from a SNP:

Illustration of an allele resulting from a SNP

Notice that the 6^th base from the left differs across all 4 people, sometimes because of the bit inherited from the mum, sometimes because of the bit inherited from the dad, and sometimes both. Because this has an effect on the protein coded for, this means that each person has a different allele of that protein gene. Using the base differences to identify the alleles, these are GG, GA, AG, and AA. (Remember that, mutations aside, these pairs of letters refer to the two stuck-together bits that make a single half-rung of the thick half-ladder; one from mum and one from dad.)

SNPs and behavioural differences

Many of the physical differences between humans result from differences in bases at particular DNA locations. Some of these occur because of the effects of one or a few SNPs, e.g., eye colour. Others result from the combined effects of lots of SNPs, e.g., height. But don’t forget that the environment always plays some role and it can play an enormous role. I don’t care how many “height genes” you have; swimming with hungry sharks is likely to take you down a peg or two.

Some SNPs (or combinations of SNPs) have mediated effects on behaviour because they affect physical characteristics that affect behaviour. SNPs that make people relatively likely to be relatively tall also increase those people’s likelihood of playing basketball at certain times in their lives, especially if they also have the “male gene” and the “American gene”. (I’m joking at the end of the previous sentence, of course. You did realise that, right? I am not doing so “randomly”. I do so to make a point. SNPs that can affect one or more characteristics are not SNPs “for” any of those characteristics. SNPs that can affect height do not result in genes “for” height. Still less do they result in “basketball genes”.)

The more closely tied a behaviour is to physical differences between people, the more likely it is that differences across people engaging in that behaviour are partly the result of SNP differences across those people. People who do and don’t do yoga are likely to have identifiable differences in their DNA (and also in their age, geographic location, social status …).

But is something like this true for “altruism”, as I use the term? Are differences in genetic code across species partly responsible for cross-species differences in having and expressing concern for the positive welfare of others? Similarly, are differences in SNPs partly responsible for differences across people in the extent to which they have and express concern for the positive welfare of others? I think the answer to both questions is almost certainly “yes” but I must leave saying why for other posts.

The question I shall move towards answering here though is, “Are there any identified SNPs which affect individual differences (among humans) in concern for the positive welfare of others?” Are there any genes such that people with one allele of the gene are more likely to manifest some discernible form of concern for the positive welfare of others than are people with a different allele of that gene? Has anyone proposed a candidate for the (inappropriate) title of “The Altruistic Gene”?

“The altruistic gene”

Seekers of the altruistic gene have typically not worried too much about what altruism is or how it manifests itself. Instead, they have tended to identify individual differences in some behaviour and claim that it is a good marker of altruism, e.g., giving away some of the money an experimenter gives you after she invites you to share it with a stranger and then watches to see what you do.

When looking for “giving money away in dictator game” “altruism” genes, researchers also often look for alleles that cause individual differences in something physical that (at least sometimes) correlates with their behavioural marker of altruism. Thus, researchers look for SNPs associated with individual differences in the production or regulation of some or other alleged “altruism drug”, such as dopamine, serotonin, testosterone, or vasopressin. The most heralded potential altruism drug in recent years has probably been oxytocin.

I haven’t the time (or frankly the inclination) to look at all the research in this area. Instead, I shall discuss a single study that seems to be fairly representative of such research.

“The (allegedly-altruistic) OXTR gene”

Oxytocin is a hormone with all sorts of effects. How to best categorise those collective effects is a matter of some debate but oxytocin seems mainly to sensitise people to social cues and often accentuate or otherwise modify their responses to them.

People have oxytocin receptors (OXTRs) throughout the body, as might be expected when oxytocin levels have such divergent effects. One SNP involved in the construction or regulation of oxytocin receptors is polymorphic: it can take different forms that influence the nature of the gene that results. This means that the OXTR gene has alleles.

Because the DNA variance under discussion occurs in a single SNP, the OXTR gene’s alleles can be described using the possible base combinations in that SNP. These are AA, AG, GA, and GG.

Participants in a study by Kogan et al. (2011) watched short and silent video segments of each of 23 people whom I shall refer to as the “lovers”. In the video clips, each of the lovers was shown listening to his or her romantic partner who was talking about “an experience of personal suffering” (p. 1910). Research participants then rated how “trustworthy, compassionate, and kind” each lover was (p. 1911). Let’s keep things simple and call this a rating of how compassionate or altruistic the lovers were thought to be.

Lovers were tested for which OXTR allele they had.

Those with the GG allele received slightly higher average ratings for compassion than did those with any of the other alleles. Furthermore, of the 10 lovers with the highest compassion ratings, 6 had the GG allele. Of the 10 lovers who received the lowest compassion ratings, only 1 had the GG allele.

The experimenters had an extra couple of people watch the video segments and rate each lover’s non-verbal behaviour: how many times they nodded, extent of eye contact, openness of arm posture, and whether or not they smiled. These rating were then combined into a single “affiliative cues composite”. 

Lovers with the GG allele were judged to display more affiliative cues than those with the other alleles.

Mediation analysis suggested that lovers with the GG allele were perceived to be more compassionate than people without the GG allele because the former displayed more affiliative cues than the latter.

Thus, Kogan et al. (2011) provided evidence that some differences across people in how compassionate they are may result, in part, from “genetic differences” between people which affect their display of affiliative cues.

A critical point

One of the things I care most about as a university tutor is encouraging students to evaluate evidence and develop arguments towards a justified conclusion. One major obstacle to this occurs when people believe without question what they read in the (mainly titles, abstracts, and summaries of) scientific literature. Sometimes it feels like all I do is shatter my students’ beliefs. This can be wearing; for them and for me. Nevertheless, I would rather they adopted a Socratic acceptance of ignorance than a set of Emperor’s false beliefs. To that end, here are some things that people might like to think about if they are tempted to report findings from Kogan et al. (2011):

1.      How confident can we be that the tales of personal suffering lovers were listening to were more or less comparable, e.g., in terms of how intense the described suffering was or how distressed people were when talking about it?

2.      Is it possible that people with different OXTR alleles attract different sorts of romantic partners, who perhaps have different experiences or ways of talking about such experiences?

3.      Was perceived compassion measured on a single rating of “trustworthy, compassionate, and kind” or the average of three separate ratings of “trustworthy”, “compassionate”, and “kind”? Does it matter either way and does it matter if you can’t find out from the paper?

4.      Did this scale/these scales run from 0 – 6 or 1 – 7? (Answer given below – but not in the paper.)

5.      Did the scale/these scales indicate how compassionate the lovers were thought to be in the specific situation they were judged, in general, both, or neither? How reliable and valid a measure do you think the scale was/these scales were of whatever your previous answer suggested?

6.      Lovers with the GG allele received an average compassion rating of 4.21and lovers with the other alleles received an average compassion rating of 3.80, a difference of 0.41 on a rating scale which ran from 1 = “Not at all” to 7 = “Extremely”. Impressed?

7.      What do you make of the fact that, of the 10 lovers with the highest compassion ratings, 4 did not have the GG allele and of the 10 lovers who received the lowest compassion ratings, one did have the GG allele?

8.      Assuming that the study’s results were persuasive in all respects, would they persuade you that people with the GG allele are relatively likely to be highly compassionate, that people without the GG allele are relatively likely to be without compassion, both, or neither? If you think the first two options are identical, think again.

9.      Do different OXTR alleles lead to differences in compassion, differences in how compassion is expressed, or differences in affiliative behaviour?

10.  Allele effects were examined among a sample of (only) 23 lovers. How reliable and generalizable does that seem to make the study’s main findings? Hint: See here

11.  How many lovers had each allele? When you’ve answered this question, maybe revisit the previous one.

12.  Were differences in scores on the “affiliative cues composite” mirrored by differences on each component of that composite? Why might it matter?

13.  If differences in oxytocin levels affect differences in a particular behaviour on a particular occasion, does this mean that oxytocin differences (a) always result in comparable behaviour differences or (b) are always involved when there are differences in the behaviour? (Hint: Adding a little salt can change the way something tastes.)

14.  Hopefully you will by now be asking yourself all manner of additional pertinent questions.

15.  When I emailed Kogan with questions similar to some of those above (and told him that I was doing so in preparation for this post), he graciously replied and admitted, “In reality, I'd say the [OXTR] gene is associated with slightly less prosociality among A carriers who are caucasian--it gets a lot dicier when you look at other ethnicities. But the effect is almost certainly small (we got lucky in our paper that it was as big as it was!).”

I’m not picking on this paper, particularly. Most of the papers I look at in detail when they claim a link between some or other “gene” and “altruism” are often even less compelling. As I said before, this can be wearing for all involved. Sorry.

Conclusion

The phenomenon I am interested in is a sprawling shape-shifter. People can have and express concern for the positive welfare of others in a multitude of ways and accordingly it can be difficult to identify reliable and valid indicators of even specific instances of such concern. Lots of characteristics influence whether and how a person will engage in even a particular instance of altruism.

Being compassionate when listening to a loved one report a distressing incident is not a single, simple, or uniform activity. It involves attending to the other; trying to understand what they are saying; trying to understand how they felt during the recollected incident; trying to understand how they feel right now; perhaps trying to work out how they might feel in the near and more distant future, perhaps as a result of things that you consider doing; wondering what you can do that would be in their best interest and not make things worse for them; managing one’s own thoughts and feelings in service of the other’s welfare; etc. How such compassion is expressed and how it can be most effective depends on one’s own abilities and preferences; what the other person likes and responds well or badly to; the specific setting (e.g., who else is around and what role they seem likely to play); etc.

I therefore do not expect simple relationships between any SNP and any single manifestation of altruism; still less any and all instances of altruism. This is not because small DNA differences can’t have huge physical and behavioural consequences. I think they can. It is because I think that altruism is too complex a phenomenon to be well predicted by a single simple indicator, whether that is an SNP or levels of some biochemical such as oxytocin.

Any search for “the altruism gene” seems to be to be highly suspect and any claim to have found it considerably more so. Whenever I have looked in detail at the evidence for such a claim, I have always found it to be seriously wanting. Given what I have already said, it would be astonishing if it were otherwise. From my point of view, studies in this area cause confusion more than they further knowledge. They give people the illusion of evidence for their false intuitions and they require a lot of time and energy to try to counter (or even to ignore).

Maybe time and good science will prove me wrong. Until then, I advise extreme caution (to the point of quite radical scepticism) in response to any claim to have identified “a” let alone “the” altruistic gene.

Prelude to later posts

As I predicted, I have run out of time long before I have run out of things to say. For now, I recommend that any of my students thinking about writing an essay using material from this week should seriously think about the following:

·        Many “genetic relatedness” studies show links between (unspecified) “genes” and individual differences in “altruism” within the sample studied. Don’t mix up potential causes of a specific instance of individual differences in altruism with reasons for group (including temporal) differences in altruism; and still less with causes of altruism. Do consider how much “non-genetic” variation there was within any given sample and how well that represents “non-genetic” variation beyond it. (If there is limited environmental variance and individuals’ differing life-experiences are not measured, of course differences in “genes” are going to explain the lion’s share of whatever differences there are in the criterion variable.) Do think carefully about the indicator of altruism and its relation to concern for the positive welfare of others.

·         Most discussions about “biological altruism”, “evolutionary altruism”, “reproductive altruism”, and the like are about a completely different phenomenon to the one studied on this module. Roughly speaking, that phenomenon concerns a living thing having a characteristic which, over the lifespan, has the consequence of being ‘costly’ specifically in the sense of curtailing how many copies of its own “genes” exist in subsequent generations. (“Genes” is in quotes because the term is used in a different way than described above for “protein genes”.) Such a hypothetical phenomenon could, if it existed, seem to cause a problem for Darwin’s theory of (individual level) natural selection. Evolutionary arguments that claim to solve “the problem of altruism” do so by explaining (away) that sort of so-called altruism (which would be better termed something like “DNA-reproduction curtailing”). Because they use such a stupid term for the phenomenon they are most interested in, the evolutionarily-inclined often get themselves and others into terrible and massively costly (in real terms) messes. Discussions about such things as “group selection”, “kin selection”, “reciprocal altruism” and the like are largely arguments about how natural selection works. Those theories were not intended to say anything about altruism as normal people understand the term: (‘psychological’) aggression is at least as likely a candidate as (‘psychological’) altruism for being DNA-reproduction curtailing. If you want to use such theories in that way (although I think you would need a good justification for doing so), you must address various issues.

o   What specific characteristic are you talking about? Describe it as objectively as possible, ideally without importing any “motive-inviting” terminology. “Makes a distinct sound when a predator approaches and in the presence of relatives” is much less likely to lead to confusion than is the phrase “Gives an alarm call” (“gives” and “alarm” both inviting confusion). If you must use something like the latter, define it well first (paying particular attention to the contexts in which the characteristic manifests) and put at least the first use of the phrase in scare quotes.

o   What evidence is there that individual differences in this characteristic are influenced by individual differences in DNA? If there is none, you are making an assumption and you need to provide justification for doing so. A belief that “they must be” because “everything is genetic” is not enough. Unless individual differences in the characteristic you are considering are influenced by individual differences in DNA, you are looking in the wrong place for a good explanatory theory for the former.

o   What evidence is there that individual differences in the characteristic can be DNA-reproduction curtailing over the life-course (seeing here, for example, and allowing for possibilities suggested by reciprocal altruism, kin selection, group selection, etc.)? If you just tell a story about how the characteristic ‘must be’ costly for DNA-reproduction, I bet I can usually come up with an equally plausible story for why it might not be. I will want reasons for thinking your Just-So story is better than mine. (For introductions into Just-So stories in evolutionary theory, you could do a lot worse than looking here or here.)

·         Evolutionarily-speaking, “altruistic punishment” is, if anything, a more misleading term than “biological altruism”. It is necessarily “altruistic” only in the “apparently curtails DNA reproduction” way, just as “evolutionary spite” would - were it to exist. (Relevant research often muddies the water by examining situations in which people pay economic costs apparently to punish violation of norms that, if followed, would benefit others in some way. The mish-mash of different types of costs and benefits – let alone inferred motives - in such paradigms almost guarantees confusion.) Again, such phenomena and possibilities may (but I would guess probably don’t) cause problems for one or other theory of natural selection. They have nothing obvious to say about people’s concern for the welfare of others.

Picture credits

All gene diagrams [Link]

Bullshit poster [Link]

Jean Genie [Link]

How to cite this blog post using APA Style

See: http://owl.english.purdue.edu/owl/resource/560/10/

T. Farsides. (2014, October 26). The genetics of altruism. Retrieved from http://tomfarsides.blogspot.com/2014/10/the-genetics-of-altruism.html