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Genes, Brains, and Being Social
(excerpts for discussion)
"If a person suffers the small genetic accident that creates Williams Syndrome, [s]he'll live with some fairly conventional cognitive deficits, like trouble with space and numbers, but also a strange set of traits that researchers call the Williams social phenotype or , less formally, the 'Williams personality': a love of company and conversation combined, often awkwardly, with a poor understanding of social dynamics and a lack of social inhibition.
The low IQ ... ignores two traits that define Williams more distinctively than do its deficits: an exuberant gregariousness and near-normal language skills ... appear to truly lack social fear ... see all faces as friendly ... fanciful verbosity accompanied by infectious affability
Because ... many of us feel uneasy with people with cognitive disorders, or for that matter with anyone profoundly unlike us ... people with Williams can have trouble deepening relationships ...
Developmental psychologists sometimes call the social urge 'the drive to affiliate.' ... the Williams deletion left it unfettered. But how do missing genes steer behavior toward gregariousness and engagement? ...
a central lesson of Williams and, for that matter, modern genetics: genes do not hard-wire people for certain behaviors. There is no gene for understanding calculus. But genes do shape behavior and personality, and they do so by creating brain structures and functions that favor certain abilities and appetites more than others ... M.I.T math majors aren't born doing calculus and people with Williams don't enter life telling stories ... 'It's not just 'genes make brain make behavior.' You have environment and experience too.'
As an experiment of nature, Williams syndrome makes clear that while we are innately drive to connect with others, this affiliative drive alone will not win this connection ... To bond with others we must show not just charm but sophisticated cognitive skills ...
gossip accounts for about two-thirds of our conversation. All this yakking - murmured asides in the kitchen, gripefests in the office coffee room - yields vital data about changing alliances; shaking machinations; new, wished-for and missed opportunities; falling kinds and rising stars; dangerous rivals and potential friends. These conversations tell us ... what our gossipmates think about it all, and about us, all of which is crucial to maintaining our own alliances ... For we are all gossiped about, constantly evaluated by two criteria: Whether we can contribute, and whether we can be trusted. Your teammates hope you'll contribute skills and intergroup competitive spirit - without, however, offering too much competition within the group, or at least not cheating when you do. They know you can't afford not to compete, and worry you might do it sneakily.
The bigger the neocortex, the higher the rate of deceptive behavior. Our extra-big brains allow us to balance bonding and maneuvering in more subtle and complicated ways ... People with Williams, however, don't do this so well.
One of the most vexing questions raised by both Williams research and the social-brain thesis is whether our social behavior is driven more by the urge to connect or the urge to manipulate the connection ...
It is possible, in short, that people with Williams miss social subtleties not just because they lack cognitive tools but because they also lack a motivation - fear of others - that the rest of us carry to every encounter ...
The dissociation of so many elements in Williams - the cognitive from the connective, social fear from non-social fear, the tension between the drive to affiliate and the drive to manipulate - highlights how vital these elements are and, in most of us, how delicately, critically entwined ..."
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Comments
To be or not to be (social)?
I was wondering... I have not read the whole article, only the excerpts above, so maybe my thoughts are somehow dissociated from the central point. I do not feel the "drive to affiliate", that social urge. In fact I seek exactly the opposite. I wasn't always like that. My genetic predispositions (hypermetropia, astigmatism, squint) have shaped who I am now, not determining my social fate, but giving the basic elements to make other so-called "normal" (at least concerning visual skills and facial esthetics) treat me as a "stranger". During my childhood I had to deal with all sorts of embarassments ("why is your eye like that?","are you blind?","poor girl, she'll never get a boyfriend..." and so on), so I focused all my efforts in studying and being alone, in order to avoid those situations. Eventually, at my 20's I had a corrective surgery for the squint that did not work very well (I had already developed amblyopia, my brain was unable to see with my left eye) and exchanged the thick glasses for contact lenses. But the social damage was already done. I have a strong desire to connect to people but I seem to be unable to know how to do it. So I stick with the other sort of animals, my dogs, the only friends I have.
This is just an example or illustration of the genetic-environment indissoluble union.
The "drive to affiliate" and its relation to social life
Your thoughts are not at all "dissociated from the central point." Very much to the contrary, they speak directly to the central point of the article as I read it: the complexity of the gene/environment interactions as they bear on human social life. Many thanks for sharing your story here. My guess is that most people, like you and I, have some significant degree of "drive to affiliate" and that their problems and successes at doing so have a lot to do with how other people/living organisms respond to them. For more along these lines see
Being an "one-eyed on the spectrum with a slippery brain "
Thank you very much for the answer and the links. I literally cried after reading the excerpts of the book "Look Me in the Eye", an evidence that people "on the spectrum" can be very emotional. I was never able to look someone in the eye. I always thought this had to do with my almost useless left eye (squint), but now I wonder if this has a much more complex explanation...
I will read these books and keep checking the comments on this site, I wish I could talk to all of you personally, but I live in Brazil!
being one-eyed and ...
Glad it was helpful. You might also find interesting Culture as Disability, about, among other things, the relation between being two-eyed, one-eyed, and blind. Brazil is ... far away in geographic space, but not so far in virtuality. Send Serendip a note at /cgi-bin/comments and let's see what we might do to bring Serendip and Brazil still closer?
A bit off-topic
Thanks again for the link and kind words. I have a question and don't know exactly where to post it... Do you have any information on "metopic suture" or "sutura frontalis persistens"? I have this thing... my skull has this open line in my forehead, about 5 mm wide. I searched the internet but the only interesting articles are in German. I would like to know if there is any link between this skull feature and other "symptoms". I also have no frontal sinus or sinus frontalis.
brain positioning
Humans have an anterior positioned brain. Is there any advantage to this?
Nature vs nurture
The argument about how much of our personality is inherited has been raging for decades - and in each generation, a 'politically correct' response appears to have prevailed. If nurture is most important, then government spending is worthwhile; if genetics is all-important, then are people 'doomed' to repeat the maladaptive patterns of their ancestors that nurture cannot undo?
There is another social myth at work too: if someone is lacking what appears to make others 'normal', such as Downes syndrome, then they must have other characteristics that make up for it, such as a nicer, 'more lovable' personality.
In this article and series of rejoinders we see scientific research at its best - a quest for facts based on real-life evidence, rather than the miasma of emotion and the rigidity of political correctness.
Congratulations on a fascinating argument!
Genes, behavior, society
As the article makes clear, Williams Syndrome raises a number of interesting issues about genes, brains, and behavior, particularly in the social realm. But before getting into those, what impressed me particularly is the article itself. Dobbs does an unusually good job of writing about the relation between genes and behavior, displaying a sophistication in this realm that other journalists would do well to take as a model, irrespective of the particular subject they are writing about. As Dobbs makes clear, in this case (and others) genes INFLUENCE behavior; they do not DETERMINE it.
There is still a tendency among journalists, readers, and even many biologists to understand from observations showing similarities in behavior among people with similar genes that genes create behavior, that we are fated by our genes to behave in particular ways. The underlying presumption is that such observations answer the question of whether it is genes or environment that is responsible for behavior: if genes then not environment (and vice versa). As Dobbs makes clear, this is imply not the case, with Williams Syndrome or anything else. If A then not B is not a valid presumption in thinking about the relation between genes and behavior. Showing that genes affect behavior leaves entirely open the question of whether environment (and perhaps other things as well) ALSO affects behavior (and vice versa; showing an effect of environmen does not preclude there also being an effect of genes). In the case of Williams Syndrome, additional observations clearly show this is in fact the case.
The point is not simply that genes and environment (and personal choices) invariably interact to produce behavior but that one cannot, from any given set of observations, say anything even remotely definitive about the relative significance of different contributors. If the amount of environmental variation present in a given population is relatively low, then genes will appear to have a big effect on behavior. If the amount of genetic variation is low, then environmental factors will appear to have a big effect. The only way to find out how much effect environmental variation would have on people with the Williams syndrome genetic variation (or any other) is to explore a variety of environmental variations (cf The Bell Curve: Issues of Individuality and Education). Genes are not "fate"; they are a starting point for an ongoing process of becoming whose possibilities remain to be determined.
Despite knowing with some precision what the variation in genes is in those with Williams Syndrome, we still don't know what those genes are doing and how much what we observe is influenced by experience. Is it an urge to use language that drives hypersociability or the other way around? Is the "gaze" a result of the gene variation or something that develops as a way of dealing with experiences that result from the gene variation? These sorts of questions help to make it clear that genes are not in people with Williams Syndrome what they are but only the starting point from which what they are emerges. And the same complexity holds for all aspects of behavior in all of us.
Dobbs not only makes clear the complexity of gene/environment interactions but also appropriately emphasizes that Williams syndrome is not adequately or appropriately characterized simply as a "deficit"; it "predisposes a person not just to weakness in some functions but also to relative (and possibly absolute) strengths in others." Here too Dobbs would well serve as a model for journalists (and others) thinking about a variety of related situations. We all have a tendency to characterize others (and ourselves) in terms of deficiencies, forgetting that we are all complex and different blends of weaknesses and strengths. And we would probably all do better if we paid at least as much attention to the latter as to the former. It would probably make us feel better about ourselves, as well as more willing/able not only to help others but to learn from their distinctive characteristics (cf. The more I learn, the more I realize more and more that how I think and feel is different and An Unquiet Mind and Culture as Disability).
This is turn brings me to ways that observations on Williams Syndrome can contribute to thinking about the brain and social interactions. Here too I think Dobbs has provided an exemplary piece of journalism, not only effectively describing observations and the interpretations that scientists making the place on them but using both to tell a story that goes beyond the observations and stories of individual scientists and invites a reader to ask new questions and create their own story.
What struck this reader particularly is the way that observations on Williams Syndrome can help in "unpeeling the onion" of "sociability", ie dissecting the several different nested meanings of this term as it is commonly used. That Williams children display a strong motivation to interact with others and yet have trouble forming successful social bonds seems to me both sad and particularly significant, implying clearly that there is more to "sociability" than simply the wish to be social. The suggestion that the barrier to effective social interactions is more about the receiver of social overtures than the sender, and that many receivers evaluate the worth of social interactions in terms of contributions to social status (hence making interactions with Williams children less appealing) is an intriguing one, perhaps related to difficulties that people on the autistic spectrum also have with "neurotypicals". Both suggest that there are two dissociable levels of "sociability", one related perhaps simply to enjoyment of interaction and a second related to the use of interaction to test and revise social status.
Adding in my own informal observations, I'd suggest that there may be at least two other distinguishable aspects of sociability. Many people seem to use social interactions as a way of stabilizing their own sense of personal identity, irrespective of the positioning it gives them in social hierarchies. And some people seem to use social interactions (story sharing) as an essential ingredient of ongoing exploration, a way of discovering new things that one might not have discovered onself.
My guess is that sociability, like all other human characteristics, will prove not only to be a complex blend of different things when looked at from the perspective of the brain but will prove to involve different blends of the different characteristics in different people. The broader challenge, it seems to me, is whether we will all learn to accept this kind of variation as not only the "norm" but as something to be appreciated for the new opportunities it creates. My one concern about Dobb's article is that it ends on a note that threatens to undercut all that has come before. Could there not be in "sociopaths" the same sort of mix of "weakness in some functions but also to relative (and possibly absolute) strengths in others" that there are in Williams people, and in the rest of us?
Response to The Gregarious Brain
Up until I read this article I had never heard of Williams syndrome. Being personally interested in social neuroscience I was excited to have an introduction to this syndrome and its possible contributions towards understanding social behavior.
I was glad this article described behavior as a function of both genes and the environment. I think it is beneficial to understand that our actions reflect neural circuitries that have been shaped by innate predispositions, but that these are merely “predispositions,” that we are not “hard-wired” for particular patterns of behavior. These predispositions significantly influence how we engage within our environment (“the endless string of challenges and opportunities that life presents any person starting at birth”), and through our experiences within our environment particular neural connections are strengthened/reinforced while others degenerate. I find this view of behavior to be valuable for a few reasons. First, this goes beyond nature vs. nurture, beyond a simple reductionist understanding, and instead stresses the important interplay between the two. It is this interplay between predispositions and our environment that we should examine if we want to better understand from where patterns of behavior arise. How do our predispositions shape how we engage within and thereby shape our environment? And how in turn does our environment shape our behavior/engagement? Second, because we are not hard-wired and fated for a particular pattern of behavior, we thereby have the ability to change who we are. While “what [one] learn[s] is shaped by the inclinations and abilities [one’s] genes create,” with work and effort, one can still learn/strengthen neural connections that their predispositions may not have lead them to strengthen. One should consider how much influence our predispositions have over how we live our life, and how much we are capable of going against them. I
was also interested to read about the emotional abnormalities associated with Williams syndrome and their implications for social behavior, connecting to work by Demasio. According to this article, research has found a dead connection between the amygdala, associated with fear, and the orbitofrontal cortex (OFC), associated with prioritizing social behavior, in Williams patients when faced with potentially threatening social situations. The research suggests that this may be a system evolved to warn individuals of social threats. From this researchers infer that “it is possible, in short, that people with Williams miss social subtleties not just because they lack cognitive tools [e.g. theory of mind] but because they also lack a motivation – fear of others – that the rest of us carry to every encounter.”
Similar to Demasio, this research suggests that emotions are key to one’s successful operation within a complex social setting. In this case it is fear along with the desire to connect with others that drive social interactions. Does this theory speak to Demasio’s somatic-marker hypothesis? I’m not sure how well they cohere, but both involve frontal cortices, the amygdala, and emotion. Simply, the somatic-marker hypothesis suggests that the feeling of emotions from previous experiences allows one to make decisions within a social setting more efficiently through ruling out possible courses of action before conscious deliberation/reasoning even takes place. Lacking a connection between the amygdala and OFC, perhaps Williams patients are unable to form some of the negative somatic markers that would otherwise warn them not to select a particular social response; they would lack an inhibitory gut feeling. However, would a lack of social fear actually prevent somatic markers from forming? Perhaps the markers do still form, but the lack of fear prevents one from attending to those markers. That is, maybe without social fear one feels that inhibitory gut reaction, but is not responsive to it. I do not understand the neural machinery underlying these systems well enough to really say, but it does seem that emotions play a key role in organizing behavior within complex social networks and should therefore be studied further.
social issues
I remember learning in educational psychology about people who have trouble socially. I don't believe we put a name to it, but if I were to name it, I would say that it's Williams Syndrome. It's interesting to me that some one who actually likes to socialize and be with people could behave in a way that would essentially push the very people they wanted to be with away. It makes you wonder about the idea that:
The bigger the neocortex, the higher the rate of deceptive behavior. Our extra-big brains allow us to balance bonding and maneuvering in more subtle and complicated ways ... People with Williams, however, don't do this so well. One of the most vexing questions raised by both Williams research and the social-brain thesis is whether our social behavior is driven more by the urge to connect or the urge to manipulate the connection ...
What are people's motives to communicate? When and why do we enjoy talking with others? Can this be relating to that person who annoyd you because they just won't be quiet? Or that old person who just keeps on telling their stories over and over again?
In response
I’m having a difficult time seeing the major, unifying point of these excerpts from the paper. Is the author’s main point that nature and nurture both have an effect on behavior? Or is it looking into how genes affect behavior and what a lack of certain genes in a small subset in the population tell us about those genes? I agree with the author when he says that genes and the environment both affect our development but I don’t see how that fits into this discussion. A developing fetus with the gene deletion along chromosome 7 that causes the syndrome WILL have the syndrome. That’s it. There is no known behavioral therapy to correct the underlying problem since it is a genetic disorder, if you want to think of it as a problem that needs to be corrected. We know by now that the brain retains some degree of plasticity throughout life but in the case of those with William’s syndrome it is a matter of certain information that is part of normal social functioning just not being there. Your environment can’t change that, even though it can influence a lot of our behavior.
The point that Dobbs brings up about social deception is an interesting one. It seems as if relationships are impaired if one doesn’t understand more subtle social cues and is unable to manipulate others to some extent. On the other hand, it would seem as if this ability for social deception is not incredibly important. This ability is not the “reason” (if one could even use the word reason when talking about random evolutionary developments) why we have come to have such complex brains with high-functioning neocortexes. If social fear were all-important than we would have more than just a small segment of genes “coding” for it. The brain is amazing in its ability to overcome impairments and change in response to the environment. As has been said before, there are at least a dozen ways in which or mechanisms by which the brain carries out any one vital function in case one pathway is knocked out. Our brains are splendidly redundant. Yet this very complex social ability is simply lacking in people with William’s syndrome. Personally, I do not think the loss is as great as it is made out to be. We talk so often about how disabled people are actually differently-abled… How is this any different?
The question of whether we were “designed” to want connection or to want to manipulate seems meaningless to me. I think that people all too often try to explain evolutionary phenomena with straightforward logic. It reflects a poor understanding of what evolution really is, as if it is goal-directed and purposeful, more than anything. I think it’s a bit ridiculous to say “okay, here’s why the human brain is the way it is for reasons A, B and C.” That point isn’t central to the paper, though, but that aspect of it interested me.
People with William’s syndrome do serve as an interesting case study in how certain functions do or do not influence others and how a few small changes in one’s genome can carry over into pronounced behavioral and physiological differences. Our personalities seem to be single entities to ourselves and our friends, so it can be disconcerting to realize that what seems whole is actually comprised of so many different components. Things such as the way in which we interact with others is actually so fragmented that it makes me wonder how we manage to be perceive the world as coherently as we do.
In Response to In Response
The Gregarious Brain
In this article, Dobbs spends time discussing the evolutionary origins of different brain structures and the complex and not-so-complex behaviors that result using the following information:
As this article highlights, the key message deals with what used to be known as the Nature vs Nurture question. The new understanding of this old debate is that every aspect of the structure and the function of our bodies – brain included – are a result of the balance between genes and the environment.
In the case of Williams Syndrome, affected people carry genetic differences that impact the way they interact with other people. Their genes affect their brains, which affect their behavior, which affect the environment they live in, which go back by the reafferent loop to reaffect their behavior. In other words, Williams people share characteristic differences in brain structure that affect, their interactions with other people, sometimes in ways that are unpleasant to them.
Many people seem drawn to identify some “otherness” in people, some phenotypic variation that is quantifiable. This is very much the case with Williams Syndrome, where especially with the case of the Williams’ stare and the Fragile X child’s aversion to eye contact “a genetically inclined pattern of behavior is … reinforced”. From this observation however, we can draw many conclusions about the genetic and environmental role played in behavior formation in all organisms. However, while I’m comfortable with the assertion that “genes do shape behavior and personality, and they do so by creating brain structures and functions that favor certain abilities and appetites more than others”, we’ve certainly not reached the end of the Nature vs. Nurture discussion.
Paul argued in the Institute today that the Nature vs. Nurture debate is dead… completely finished. I disagree. While I think that the overarching debate about whether genetic makeup or environment exclusively influence a developing human structurally and functionally, the debate is certainly not over. I’m not convinced that each individual trait in the library of human behavior is affected by a consistent ratio of genetic and environmental involvement. It seems quite possible that the elasticity of the developing aorta or the color of a person’s hair would be more heavily influenced by genes than experience. Conversely, it seems quite possible that conceptual tasks, or as argued in this paper, our understanding to one another and our ability to listen to/share/modify stories would have a stronger experiential role in their development. It’s useful, but not sufficient to say that we’re all partially genes and partially experience when each trait might be differentially influenced by either factor.