Conversation: George Slavich on Human Social Genomics

For a while science and society has understood the relationship  between our genes and our environment as the story of genetic potential. The story goes like this: we are born with a fixed set of genes, and our environment, and our experiences in that environment, determines the level to which we realize the potential of our genetic predisposition. This story sounds plausible, and its existence is fueled by our conception of the gene-environment relationship as “nature vs. nurture” and “genes by environment”(1). However, this version of the story fails to capture the complex relationship that our genes and our social environments share.

New research, in the field of Human Social Genomics, shows that our social-environmental experiences can shape our genetic expression, throughout our life. In a recent review of the field, George Slavich and Steven Cole write that, “The human genome…is not a static blueprint for human potential. Instead, our genome appears to encode a wide variety of ‘potential  biological selves,’ and which ‘biological self’ gets realized depends on the social conditions we experience over the life course”(2).

After featuring their article entitled, “The Emerging Field of Human Social Genomics,” in the July 26th Research Lead, we spoke with co-author George Slavich to find out more about their research, which has has broad implications for how scientists and society understand illness, social networks, evolution, and even public policy.

George_Slavich_PhotoGeorge Slavich is an assistant professor and Society in Science Branco Weiss Fellow in the Department of Psychiatry and Biobehavioral Sciences at UCLA. He is also director of the UCLA Laboratory for Stress Assessment and Research. His research investigates the psychological and physical impacts of adverse social experiences. He has been the recipient of a number of awards, including the 2012 Theodore Blau Early Career Award for Outstanding Contribution to Professional Clinical Psychology.


Evan Nesterak (EN): You and Steven Cole recently reviewed the field of “Human Social Genomics” last month in the journal of Clinical Psychological Science, what is Human Social Genomics?

George Slavich (GS): Human social genomics is a term that we’ve used to describe the phenomenon that characteristics of the social environment, and even more importantly our perceptions of those conditions, appear to be able to penetrate deep inside the body to influence the activity of some of our most basic processes, namely the expression of our genes.

There has been a lot of elegant work in animal model systems showing that if you expose animals to different types of aggressive intruders or other social manipulations that you can measure differences in gene expression as a function of those conditions. But it’s only been recently that those same types of effects have been demonstrated in humans. The idea that the different social-environmental conditions that we’re exposed to can influence the activity of our human genome is what lies at the heart of human social genomics.

 The human genome…is not a static blueprint for human potential. Instead, our genome appears to encode a wide variety of ‘potential  biological selves,’ and which ‘biological self’ gets realized depends on the social conditions we experience over the life course.

EN: The standard view right now is that our genetic selves are somewhat static and that the environment either allows us to realize the potential of our genetic predisposition or not. How does human social genomics and your research change that framework?

GS: This is a really special point. We think of ourselves as being relatively stable in a genetic sense. We have the idea, based on research, that different people might be more likely to experience different diseases, or they might be more likely to act in certain ways, as a function of variation in our genetic code. We have had this idea that we’re born with our genetic code, and for all intents and purposes that code doesn’t change much over the course of our lifetime.

It’s sort of a technical point, but that’s what happens at the level of DNA. DNA doesn’t have direct effects on our behavior, because genes only influence the production of proteins when those genes are expressed. That gene expression, which involves RNA, does seem to differ based on the different social environmental situations that we’re in. That’s not obvious to us, because we don’t really have any way of knowing in our body which genes are expressed or not. But it does add a certain insight to the idea that, even though our DNA may be largely fixed and unchangeable over time, the gene expression, the production of MRNA is not, and is in fact influenced, in some cells, to a great extent by the social-environmental situations we’re in. The idea of social genomics really says that the genetic factors and the social-environmental factors are not independent, they influence one another.

EN: What are some types of experiences that influence genetic expression as you described?

GS: Of the things that have been studied so far, the types of social-environmental conditions that seem to be particularly impactful for human gene expression include, being socially isolated, or self-reporting a low level of social interaction, loneliness, and poor social connection. Also being exposed to social rejection. Some newer research is showing that even if you just expose individuals to social situations in which they’re being socially evaluated, it also seems to influence human gene expression.

Of course, we’re wondering what all of these types of situations have in common. One possibility is that the things that I mentioned–being lonely, being evaluated–that all of these conditions seem to have some implications for our social status and our social well-being. And at least historically, they might have also served as cues for the likelihood of possible physical danger.

EN: What impact might this research have on the way we think about treatment of disease and mental illness in our society?

GS: Epidemiologists and psychologists have long known that some of these factors seem to have enormous implications for health. For example, being lonely or socially isolated serves as a risk factor for morbidity and mortality that is on par with smoking and not exercising. That might sound crazy–if you’re socially isolated the risk associated with that is just as high as it is if you’re smoking. We have a similar story when we’re talking about low socioeconomic status. Individuals who are on the lowest rung of the socioeconomic ladder seem to have the worst health, while those at the highest rung on the socioeconomic ladder have the best health. Being low on the socioeconomic status ladder is tremendously risky for health. There are counties in the United States where the average life expectancy is still under 40 years old.

For a long time we’ve known that those types of social-environmental stress have a very strong effect on health. They do so by increasing risk for lots of different diseases: cardiovascular disease, rheumatoid arthritis, neurodegenerative disorders, certain cancers etcetera. But it’s remained a mystery what is happening in that big black box which is the body. How can it be? Why would it be? How could it be that those factors somehow get represented in the mind and then translated into physiological activity and immune system activity that actually leads to the emergence of certain diseases that could accelerate death?

The ideas that we talk about in the paper provide one set of pathways that might link some of these experiences of social-environmental adversity to these negative health outcomes. To the extent to which the immune system altered its activity at the level of the genes, in order to be in line with the likely experience of physical or social threat, we might have a possible explanation for how it is that these adverse social conditions can get under the skin to influence the activity of the human genome, and ultimately lead to increased risk for some of these diseases, specifically diseases that involve inflammation.

EN: Your paper also brings up the point that the impact of social-environmental experiences on genetic expression can go beyond the individual level. Can you talk more about the concept and the implications of a human metagenome?

GS: It’s a profound way to think about how we how we exist in social networks. We typically think of ourselves as being independent entities. My body is my body. Your body is your body. Although we interact in in the same social network or we travel in similar circles, we don’t really think too much about the ways in which your biology would be affecting my biology, but as it turns out one of things our bodies can do to stay biologically healthy is to tune and retune the activity of the immune system so that it is prepared to deal with possible threats in an environment. To the extent to which the individuals around you provide relatively good information of their likelihood of experiencing threat, your immune system can make sense of that information to make sure that it’s tuned properly.

En: In your review article, you explain that it is not only experiences in general, but the way an individual interprets his/her experience that really makes the difference. Someone might perceive themselves as lonely and someone might not, and that could then affect their genetic transcription? Could you explain that?

GS:Thats exactly right. The effects of all social experiences on the body are cognitively mediated. Everything that we experience is processed through our brains and then translated into different patterns of activity, physiological activity, that can therefore affect immune cells. The fact that we don’t have direct access to an objective reality and the fact that the brain is a critical linchpin in perceiving and responding to the external social world opens up the possibility that you could perceive a certain situation [differently] than I perceive the same situation.

Since the brain is the primary organ that is regulating physiological and immune system activity, then what matters is not just the life events and difficulties that we’re exposed to, but what we make of those events. That’s not to say that the life events themselves don’t matter, because the thoughts that you have are based on those life events. It’s just to say that the downstream consequences of the effects that the social world has on us are mediated by the thoughts that we have about those situations.

EN: Do you think this research could have any implications on how can we monitor people’s social-health in real-time?

GS:We have been working for four years now on developing an online system for assessing stress. In order to come to the realization that you really do need to reduce the amount of social adversity in your life you have to know what that level of social adversity is. We think that being able to measure social-environmental adversity is really the first step to being able to deal with some of these stressful life experiences.

EN: What is the next step for the research?

GS:We’re just starting and other groups are just starting to conduct studies that involve manipulating the social environment in the laboratory to document that it’s actually the exposure to these social threats that are causing the transcriptional shifts and not the other way around. Another line of research is to look at interventions that could inoculate people from experiencing the negative consequences to these different adversities.

EN: Is there anything else you would like to add to our discussion?

GS:The only other thing that I could add is the idea of social signal transduction. Its been implicit in everything that you’ve said.  For a long time we haven’t really known the set of mechanisms that link our experience of the world with the activity of our genome. What the concept of social signal transduction does is it provides a blueprint for trying to understand the entire pathway;  the mechanistic pathway that links the experience of the world with the activity of our genome. And the activity of our genome with our experience of the world.

We’re not just trying to understand how adverse conditions affect the activity of the genome, but we’re also trying to understand the entire biological pathway by which experiences of the social world affect the activity of our genome. All of the different steps that include neural processes, physiological processes, molecular processes, and genomic processes. Where some of the most exciting work will come in the future is insights into understanding exactly each of these mechanisms, and then trying to use that information as leverage to find new ways to alter the functioning of the system to improve health.


Further Reading (Click citation for link to full pdf)

Review of Human Social Genomics
Slavich, G. M., & Cole, S. W. (2013). The Emerging Field of Human Social Genomics. Clinical Psychological Science, 1(3), 331-348.

Genes and Well-Being
Fredrickson, B. L., Grewen, K. M., Coffey, K. A., Algoe, S. B., Firestine, A. M., Arevalo, J. M., … & Cole, S. W. (2013). A functional genomic perspective on human well-being. Proceedings of the National Academy of Sciences.

Human Social Genomics and Stress Management  in Cancer Patients
Antoni, M. H., Lutgendorf, S. K., Blomberg, B., Carver, C. S., Lechner, S., Diaz, A., … & Cole, S. W. (2012). Cognitive-behavioral stress management reverses anxiety-related leukocyte transcriptional dynamics. Biological psychiatry, 71(4), 366-372.

Social Isolation Influences Genetic Expression
Cole, S. W., Hawkley, L. C., Arevalo, J. M., Sung, C. Y., Rose, R. M., & Cacioppo, J. T. (2007). Social regulation of gene expression in human leukocytes. Genome Biol, 8(9), R189.

Social Signal Transduction
Cole, S. W. (2009). Social regulation of human gene expression. Current Directions in Psychological Science, 18(3), 132-137.


1, 2. Slavich, G. M., & Cole, S. W. (2013). The Emerging Field of Human Social Genomics. Clinical Psychological Science, 1(3), 331-348.

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