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.)
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:
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 6th 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
T.
Farsides. (2014, October 26). The genetics of altruism. Retrieved from
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