The interface between family and genomics (2007)

Journal of Family Psychotherapy, 18(1):1-9. A previous version was published in Spanish in Perspectivas Sistemicas, 17(87):3-6, 2005

Author: Sluzki CE

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Plenary presentation, International Conference on Family Therapy AFTA-IFTA 2005,
“Politics, Community and Clinical Practice.” Washington DC, June 2005.


Carlos E. Sluzki, MD

A number of years ago two friends of mine, he a psychoanalyst and she a psychologist, had non-identical twins. I visited them a few days after delivery, and they commented to me how different those two baby boys were: one was serene, calm, would wake up with minimal fuss, breastfeed placidly and after some minutes fall back into a blissful sleep; the other, instead, would wake up attacked by demons, howling as if dying. He would remain so agitated that he had trouble finding the nipple when attempted to be breastfeed, choked with his own sobs while sucking, and, when reaching satiation or perhaps exasperation, would spit the nipple and continue to cry until falling into an uneasy sleep.

My friends commented: It is clear that one has a much better tolerance to frustration than the other. Perhaps he had already begun to internalize a good breast, perhaps his lower quota of thanatos protected him from transform his hunger into the experience of an attacking, evil breast; while the other was tormented by his low tolerance to anxiety, already at the mercy of a bad breast attacking him. Hence their resolve: They would deliver their attention to the agitated one, breastfeeding him first and soothing him as much as they could, as the other could wait without excessive distress.

A couple of days later I was visiting them again, and chatting about their resolve, they confessed that they were amazed at the stupidity of their own prior decision: if they would have fallen in the relational trap of responding first to the one with the pesty behavior, they said, they would be rewarding his disruptive antics and ultimately punishing the other one for being just a sweet baby, risking initiating a family pattern leading toward the making of a sociopath and an abandonic schizoid! So they decided to most certainly not provide preferential treatment to the agitated one, bad breast or not bad breast. They would behave ecumenically: they would offer first attention one day to one, and the next day to the other.

I will spare you subsequent parental oscillations of that couple, as my friends kept on changing frame of reference, from hard-core Melanie Klein to Skinnerian cum Bowlby with a sprinkle of family systems, and back, with the resulting shifts in their own resolve. But they were also responding to what we knew for centuries, and at the same time we regularly dismiss in our practice, namely, that we come to this world with a reasonably tight range of genetic propensities that can be amplified or dampened by whatever family, cultural and socioeconomic environment that the lottery of life provides.

My friends’ first stance had indeed some merits: there is research evidence that shows that infants who are more negative and reactive benefit the most from sensitive, responsive care and secure attachment (Gunnar et al., 1996). But my friends’ second resolve was also reasonable: A complementary research shows that infants who demand attention, positively or negatively, do better than those who appear inhibited and don’t cry, as passive babies will reduce parental involvement (Gunnar & Nelson, 1994). All this is not very surprising, considering that we all know that babies train parents, as much as than vice-versa. And there is strong research evidence that those different styles of being in the world, expressed already at birth, tend to retain their presence, with not too many variations, throughout life. That may be telegraphed to us already by the visible representation of genetic traits since birth (“Whom does she look like?”)

This presentation will focus on the interface between what we bring into the world and what the world brings to us, between genes and environment. This interdisciplinary exercise shouldn’t be new to us, family therapists. In fact, family therapy was born in an interdisciplinary environment, ready to bridge different forms of knowing, open to borrow and test ideas and models from other fields – some of them neighboring, some distant. Granted, we may have lost some of that élan. Maybe one of the unwanted byproducts of becoming disciplinary is to end up being too civilized, too constrained, mistrustful of the neighbors, becoming our own jailers. Or maybe that certain loss of identity, when the systemic view spread to become no longer a privileged lens of family therapy. That loss is just a symptom of the deep trauma inflicted upon the field by the experience of being marginalized by managed care, compounded by the NIMH’s recent “decade of the brain” and its emphasis on basic neurosciences research to the exclusion of psychosocial explorations.

Meanwhile, powerful, towering conceptual edifices were being built in the neighborhood. One of them, genomics and developmental genetics, has resulted in a recent outpouring of research with implications that defy the imagination, and that brings us good news, bad news and fresh air.

For many years genetics was a rather insular field, treating its subject as hard and stable data and the context where genes were expressed as soft and marginal. However, once accomplished the monumental feat of mapping the whole sequence of the human genome, genetics is beginning to look at its field with a systemic lens, both in its studies of inter-genes regulatory systems and sequencing and in terms of the relationship between genes expression and environment. “We have the actors,” those researchers seem to say, “but, what is the scenario, in what context do the genes express or dampen themselves? How does the genome work in the real world?” In fact, while the process of transmission of the genetic instruction follows rather predictable, Mendelian, laws, the expression of that patrimony is profoundly affected by the family style in which the individual is raised, the social environment in which that person lives, and the myriad of events that populate our lives. The edges between genes and environment – and this assumption of what is “hard” and what is “soft” – seem to be blurring, as the research literature shows that many genetic traits seem to be so sensitive to the environment while some components of the environment – cultural traits, for instance – seem so stable if not pervasive.

Last year, at AFTA’s annual meeting, David Reiss summarized some of the results of his team’s powerful ten-year longitudinal research on the influence of genetic factors and family relations on adolescent development (McGuire et al., 1994, Reiss, 2000, Reiss et al. 2001a and 2001b). As those who were here may remember, his. The evidence provided by this as well as other research projects seem to tell us, much against our professional creed, that the family has comparably minimal influence in terms of generating personality traits such as extroversion-introversion, impulsivity-control, shyness-outgoingness, interests, and perceptual bias in their offspring. But all is not lost: The family milieu is credited for its contributions to the development of self-esteem and cognitive ability, and, alas, for a quota of the offspring’s psychopathology (e.g., Mc.Guire et al. 1994, Rende et al., 1993). But, broadly speaking, study of families with identical twins, fraternal twins, regular siblings, half siblings and step siblings, a paradigmatic way of assessing the expression of the individual genetic capital in context, show that whatever similarity siblings may have seems to derive from the amount of shared genes rather than from the family environment they share (cf. also Plomin, Chipuer and Neiderhiser, 1994).In the average population, Reiss concluded, the purely genetic effect does not exceed 50%. We may choose to complain for that quota, or to acknowledge that that percentage provides the psychosocial world with more than ample turf to provide its imprinting.

Just to keep us on our toes, and to welcome more challenges to dominant views in the field of family therapy, genetically-determined behavior of children evokes in their parents the very behaviors that we assume may have caused them in their children (e.g., Reiss, 2000, pp. 7-8) – again, babies train their parents. In fact, in another project researchers were able to predict accurately the parenting style of adoptive parents of children given away at birth just on the basis of a study of behavioral traits of the birth parents (O’Connor et al, 1998.) To complicate things further, there is data to support the assertion that parental warmth, long thought to enhance self-esteem in children, may be the adult manifestation of the same genetic trait that express itself as high self-esteem in childhood (Kandel et al, 1986); that is, both high self-esteem and parental warm behavior may be two expressions of the same gene at two different periods in life. We may thus imagine a sequence of reciprocal influences by which earlier genetically-driven behaviors of the child affect the parents (who are in turn skewed by their own genetically-driven program), their response affecting in turn the child, and so on (Reiss, 2000, p.402). Luckily, the random vicissitudes of the environment and conflicting mandates of our culture introduce some welcomed chaos to this otherwise deterministic algorithm.

Even the strong assumption that parental aversive, violent behavior leads to misbehavior in their children as well as antisocial acts in their adolescents has shown to hold water only when a strong genetic component is added to the equation. Further, an elegant cross-design project studying mothers interacting with their own children and with other children may be in point: “misbehaving,” difficult children evoked similar negative responses in their own mothers and in mothers of other, non-misbehaving, children. These responses, mind you, have been frequently considered the cause of that misbehavior. Just to complete the punch, mothers of both groups displayed equally positive, caring behaviors when interacting with children that behave in a friendly, social appropriate manner (Anderson et al., 1986.)

Let us visit an area well known to us: when raised in orphanages, or raised by parents who are emotionally drained by extreme social marginalization and poverty, or consumed by drug addiction, or extremely erratic or violent, babies and small children suffer both physical and emotional hardship with long lasting consequences in their lives (Butter, Giller and Hagell, 1998, among others). This process is multi-layered: the chronic lack of parental affection in early childhood has been shown to inhibit the expression of specific genetic traits that result in an anatomically visible reduction in the development of certain areas of the brain. This is translated in turn into frequently inalterable delays and distortions in developmental markers, including their psychosocial development. All this is measurable not only psychometrically but physiologically in terms of enzyme values that in turn generate deficits, including a reduction in the immunological defenses – making the child, for instance, more susceptible to infections. However, the impact of those adversities varies substantially from child to child: hereditary traits, expressed early in life, play a significant role in moderating or increasing the sensitivity of children to environmental insults (Caspi et al, 2002.) Resilience has, indeed, a strong genetic component. Mind you, none of these observations entail linear causality; they simply complicate our conceptual lives as modelers and our clinical lives as therapists.

Another wake up call: Many of the behavioral problems and symptoms in children thought to be a consequence of divorce actually precede it (Block et al, 1986, Cherlin et al, 1991). In fact, genetically facilitated antisocial behavior in adolescents may be preceded by more subtle disruptive behavioral features in children (Lyons-Ruth et al., Tremblay et al, 1994), a trait that by itself increase family conflicts and probabilities of divorce.

A perhaps more soothing voice in the interface genetics/family comes from Pekka Tienari and Lyman Wynne’s (Tienari et al., 1985, 1987, 1994) landmark study on families who, without information about the family of origin, had adopted at or shortly after birth children of mothers with a diagnosis of schizophrenia (“high risk” from a genetic viewpoint) and of mothers without psychiatric diagnosis (“low risk”). This research explored the effect of family quality environment on the expression of psychopathology of children (both on those with higher genetic risk of psychopathology and in those without it). Adoptive families that happened to be muti-problematic showed a higher presence of psychopathology in their offspring, with an increased load in the “high risk” offspring, while families with strong relational skills and problem-solving abilities showed a reduced expression of psychopathology in their offspring, regardless of their genetic risk. In sum, this study shows that families have both a buffering effect and an enhancing effect on the genetic risk.

The field of genomic research doesn’t disclaiming the value of individual, couples, or family therapies – in fact, it can be said that it has already contributed with some interesting psycho-educational guidelines. Further, the type of research generated by that field of inquiry is simply not designed to explore whether family interventions can enhance health promoting genetic traits or neutralize pathogenic ones, or any question like that. Those issues require our contribution, and constitute an open challenge for the field of family research, theory building and therapy. To choose to accept it requires, as I mentioned already, to be ready for an extremely humbling reassessment of many of our cherished assumptions about family causality and ultimately a revision of our definition about the nature of interpersonal problems and their resolution. If and when we work through that wound to our isolationist omnipotence, we may begin to retool our models and practices so as to grow in harmony with, and enrich, astounding advances that are taking place, with us or without us.

A thoroughly integrated, systemic view that intertwines genetic tendencies, genomic interplays, neural developmental processes, psychological maturation, emotional development, interpersonal processes and social dynamics may be still in the future, but is already beginning to be built, slowly, step by step. To choose to participate in that endeavor will reward us with the extraordinary opportunity to expand our view of the human condition... and to sooth good people like my friends, caught otherwise in the illusion of a nature-nurture split.


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  1. This benefit is not merely observational, but measured in terms of titration of cortisol, a stress hormone that at high levels arrests brain development, while its production is buffered in supportive secure contexts (Gunnar, 1998). Another fascinating line of research, this one on the behavioral and neural effect of maternal care in laboratory animals as well as its sustained effect across generations can be found in the work stemming from Meany and his collaborators (cf., e.g,, Fish et al, 2004).
  2. “Genomics” is generally utilized to refer to the studies of the genetic set, as a dynamic and evolving system that includes the influence of biological pathways, physiologic processes, and the environment in all its dimensions. “Genetics” tends to be used to refer to the study of single genes and their expression. 
  3. Needless to say, most genes and environment studies focus on an average population, not on extreme cases – such as deprived, depriving, maltreating or awkward families, where their impact in terms of severe distortions of the physiologic and psychosocial development are detected in their offspring since early in life.
  4. Even the probability of divorce may be predicted on the basis of traits with a strong genetic contribution, such as those that lean people toward an aggressive style – a risk factor – or a traditionalist stance – a protective factor for marriage (Jocklin et al., 1996, McGue and Lykken, 1992.) We may already know much of that intuitively, but to firm some of our intuitions in substantive research and to discard others as mere superstition may help us to rethink some approaches to couples’ therapy.
  5. This same observation has been made with adopted offspring of biologic mothers with depression (Kendel et al., 1995).
  6. Echoing Norbert Wetzel plea during the 2004 annual AFTA meeting, to “continue (…) the discourse between our different professional worlds with the intellectual audacity in the tradition of the Enlightenment” (Wetzel, 2004).
  7. Family therapy as and exploration of genetically favored personal/interpersonal styles of family members and a calibration of best possible fits? As a search of a story that would harmonize genetic proclivities, personal styles and events? A blurring of the boundaries between psychoeducational and systemic approaches?
  8. A valuable interdisciplinary stance – with a strong attention to genetics – has been advocated and enriched steadily by colleagues representing the integration between family therapy and medicine, under the flag of the bio-psycho-social approach (Frankel, Quill and McDaniel, 2003), as well as many contributions chiefly published in the journal Family, Systems and Health.) Cf. also the March 2005 issue of Family Process, where both John Rolland and Janet Williams (2005) and Susan McDaniel (2005) offer insightful discussions of the way families are affected when one of its members presents or is at risk of presenting a genetically-driven disorder, as well as an orientation toward a family approach to genetic counseling.
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